Repetitive Head Injury Syndrome

Repetitive Head Injury Syndrome

In this article:


Primary head injury can be catastrophic, but the effects of repetitive head injuries must also be considered. Second-impact syndrome (SIS), a term coined in 1984, describes the situation in which an individual sustains a second head injury before the symptoms from the first head injury have resolved.

The second injury may occur from days to weeks following the first. Loss of consciousness is not a requirement of this condition, the impact may seem relatively mild, and the athlete may appear only dazed initially. However, this second impact causes cerebral edema and herniation, leading to collapse and death within minutes. Only 17 cases of confirmed SIS have been reported in the medical literature. Thus, the true risk and pathophysiology of SIS has not been clearly established.

Importantly, even if the effects of the initial brain injury have already resolved (6-18 mo post injury), the effect of multiple concussions over time remains significant and can result in long-term neurologic and functional deficits. These multiple brain insults can still be termed repetitive head injury syndrome, but they do not fit the classification of SIS. True SIS would most likely have a devastating outcome.

A study of American high school and college football players demonstrated 94 catastrophic head injuries (significant intracranial bleeding or edema) over a 13-year period.1 Of these, only 2 occurred at the college level. Seventy-one percent of high school players suffering such injuries had a previous concussion in the same season, with 39% playing with residual symptoms. On the other hand, results from a study of concussion by the National Football League demonstrated no cases of SIS or catastrophic head injury in players returning to play in the same game after resolution of symptoms.2

The outcome of multiple minor head injuries over a prolonged period has not been well studied and is not well understood. The preponderance of data assessing the impact of repetitive head injuries on short- and long-term neurologic (cognitive) performance has been focused on the sports of boxing and American football.1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15

Numerous studies of professional boxers have shown that repeated brain injury can lead to chronic encephalopathy, termed dementia pugilistica.12, 13, 14, 15, Likewise, the autopsies of 2 former professional football players with a history multiple concussions demonstrated changes that were consistent with chronic encephalopathy.5, 6

Another investigation of retired professional football players showed a three-fold increase of depression in players with a history of three or more concussions.3Older studies of American and Australian rules football showed no effect from repetitive mild head injuries.11 However, more recent studies of collegiate football players showed an association between multiple concussions and reduced cognitive performance, prolonged recovery, and the increased likelihood of subsequent concussions.

Evidence has also been gleaned from other sports that involve head impact. Nonrandomized studies of soccer players who have had multiple minor concussions have demonstrated that these individuals performed worse on neuropsychologic tests compared with a control group.16, 17, 18, 19

Neuropsychologic testing is the standard for monitoring cognitive recovery after concussion. However, two studies suggest that abnormalities in visual motor and motor cortex function persist after neuropsychologic testing has normalized.8, 20 Slower recovery in patients with a second concussion was also seen.

Basic science research is also ongoing. Experiments in concussed rats demonstrated prolonged abnormalities in metabolic markers of brain activity when a second impact was administered at three days. 21, 22 This implies there may be a metabolic window of vulnerability to a second impact that leads to chronic or prolonged symptoms. Clinically useful biomarkers for brain injury are also being investigated.

Update on chronic traumatic encephalopathy

The effects of single or multiple TBIs in later-life are poorly understood, particularly in mild TBI (mTBI). Recent studies suggest that even mTBI can lead to an increased risk of later-life cognitive impairment and neurodegenerative disease, especially when repeated injuries are involved. 23, 24, 25 TBIs of mixed severity have been associated with an elevated incidence of Alzheimer disease (AD) and other dementias 26, 27, 28 and a reduced age of onset for AD, 29 although not in all studies. 30

It has long been suspected that repeated concussions can result in dementia-like symptoms many years after injury, a condition labeled chronic traumatic encephalopathy (CTE). The brain structures damaged in CTE are critical for memory and executive function. 31, 32

CTE has been studied in boxing, wherein retired boxers developed dementia at a higher rate and a younger age compared with the general population. 33 More recently, brain autopsies of athletes in various sports with confirmed CTE have demonstrated tau-immunoreactive neurofibrillary tangles and neuropil threads, 25, 34 suggesting that pathological processes similar to AD may be involved.

A critical gap in the literature exists with respect to later-life neuropsychological functioning after TBI. In a study of individuals with TBI of varying initial severity, researchers found later-life cognitive impairments when compared with a control group in the areas of episodic memory, short-term memory, visuospatial processing, object naming, and semantic processing. 35 Regarding CTE specifically, neuropsychological deficits have been observed but appropriate norms do not exist. 36

A meta-analysis found no cognitive effects in 289 amateur boxers 37 ; however, a large survey study suggested that multiple concussions increase the risk of later-life cognitive dysfunction. Recently, the diagnosis of mild cognitive impairment (MCI, also known as insipient dementia) and self-reported memory problems were more common among football players who reported 3 or more concussions than those who reported none. 23, 24 Although several cross-sectional studies in sports injury populations have been performed later in life, the long-term effects of TBI in nonsports populations (military, civilian) remain poorly defined.

The possibility of a link between mTBI and CTE or early dementia has widespread implications for military service members and veterans. TBI is an important source of morbidity in the ongoing global war on terrorism (GWOT). 38 TBI has been called the "signature injury" of Operation Iraqi Freedom (OIF), Operation Enduring Freedom (OEF), and Operation New Dawn (OND), affecting up to 20% of all service members deployed in theatre. More than 233,000 TBIs have been officially reported in OIF/OEF/OND between 2000 and 2012 (, nearly 80% of which are mild. 39 Explosive munitions in the form of improvised explosive devices (IEDs) have caused the overwhelming majority of these identified cases. The prevalence is likely higher than the above-reported numbers, given the frequency of blast exposure in the GWOT and the fact that mTBI may go unrecognized during and even after deployment. The Chronic Effects of Neurotrauma Consortium is $62.2 million, 5-year collaboration established in 2013 between the VA and DoD to establish a standardized research approach to investigate the long-term patterns of recovery and potential neurodegenerative effects of repeated, combat-associated concussion led through the Department of PM&R at Virginia Commonwealth University and including more than 30 academic Universities, 15 VA Medical Centers and 7 military treatment facilities across the U.S. 40

Missed or delayed diagnosis of mTBI is attributed to the subtlety of symptoms, the overlap of clinical signs and the common effects of heightened arousal and activity in times of combat, a lack of knowledge as to the specifics of diagnosis and detection, greater attention paid to more visible concomitant injuries, and a reduced subjective awareness related to cognitive deficits in the acute period on behalf of the injured service member. 41

At present, a definitive diagnosis of CTE is made on postmortem examination, using a battery of immunohistochemical markers to define pathognomonic histopathologic features of this disease process, such as tau-immunoreactive neurofibrillary tangles and neuropil threads. There are no clear in vivo diagnostic tools to diagnose CTE. Identification of such a tool or set of tools would provide key data to clinicians caring for this patient population, aid in conducting epidemiological studies to explore the natural history of CTE, and provide objective diagnostic endpoints to support clinical trials to explore therapies for this disease process. Much more attention in recent years has been put towards the early detection of dementia than that of CTE.

In recent years, significant effort has been devoted to the creation of imaging agents that selectively accumulate at sites of interest and emit a signal that can be detected by either positron emission tomography (PET) or single-photon emission computed tomography (SPECT). In contrast to CT and MRI sequences, PET and SPECT have the significant advantage of providing information on changes occurring at the cellular or molecular level. To date, a number of targeted imaging agents have been cataloged at the NIH MICAD Web site:

In studies of aging, sensory and motor changes have been observed that precede dementia in the domains of olfaction, eye movement, and balance. Olfactory impairment has been identified as a preclinical marker of AD. 42 Olfactory function is also reduced after brain injury. 43, 44

Researchers have recently demonstrated that early neuromotor impairments are predictive of late global outcome after TBI. 45 Using video-oculography, saccadic eye movement abnormalities have been described in patients with cortical neurodegeneration (AD) and/or nigrostriatal neurodegeneration (Parkinson disease). 46 Furthermore, eye movement abnormalities have been identified in adults with postconcussive syndrome. 47 Research has also demonstrated the utility of a mobile video-oculography device. 48, 49

Finally, balance impairments (as measured by computerized posturography (CPT) are more common in dementias of all types compared with controls 50 and have been demonstrated acutely after mild TBI. 51 CPT score is predictive of recurrent falls in persons with balance and vestibular disorders. 52

Tau proteins (collectively termed "total-tau") are a logical indicator of CTE and, more broadly, TBI-onset neurodegeneration. Total-tau in cerebrospinal fluid (CSF) is one of the most predictive biomarkers for clinical use in neurodegenerative disorders associated with cognitive impairment. 53 While serum total-tau has been less predictive than CSF for age-onset neurodegenerative disease (eg, AD), it has been demonstrated to be discriminative in other pathologic causes of brain dysfunction, including higher-risk mTBI patients. 54

Given the unique pathology associated with CTE and tau accumulation more broadly and around blood vessels, it is entirely plausible that long-term neurodegeneration following trauma may selectively present elevated serum-tau levels. It is further postulated that long-term serum-tau levels in posttraumatic subjects will be less age-dependent than CSF-tau levels in age-onset neurodegeneration. The authors’ contention is entirely consistent with the known pathobiology of CTE, specifically the excessive tau accumulations seen across broad cortical areas with a focus around blood vessels in regions of geometric inflection that are most stressed by the deformation forces of brain trauma.

CTE has also been characterized by widespread TDP-43 proteinopathy. 55 TDP-43 is involved in regulating translation in mitochondrial RNA in the brain. It has been associated with the physiological response to traumatic axotomy. 56 Blood levels of TDP-43 are elevated in association with a variety of neurodegenerative conditions, to include frontotemporal lobar degenerations, amyotrophic lateral sclerosis (ALS), and AD. 57, 58 However, no publication to date has examined it as a biofluid marker for CTE. As in the case of tau, TDP-43 fibrillaries accumulate at anatomical points of geometric inflection in the brains of CTE subjects. Given that trauma focuses deformation forces in these areas, it is highly plausible that TDP-43 accumulation is in contact with the compromised microvasculature and, as such, would be present in the blood of trauma patients with latent CTE.

Beta-amyloid (Ab) peptides are yet other biomarkers with diagnostic and prognostic utility for a broad number of neurodegenerative disorders. 53 Ab plaques are common immediately after TBI, 59 and Ab continues to accumulate in traumatized axons that survive. 60 Recently, it has been reported that Ab plaques are diffusely yet widely present throughout the brains of moderate-to-severe TBI subjects at 1 year or longer following injury. 59 Plaques were also found to be predominantly in a fibrillary form that resembled AD pathology more than acute TBI. Importantly, diffuse, widespread fibrillary Ab accumulation resembles CTE pathology. 61 Until recently, CSF has been the only biofluid found to provide reliable Ab measures. However, the latest blood Ab assays are providing predictive and prognostic performance in MCI and AD that is considered particularly useful for longitudinal monitoring and so it holds relevance to the present application. 62

While blood assays are most often developed for disease biomarkers, urine provides certain distinct advantages. Precedence exists in the form of a urine assay for neural thread protein (NTP), which is already available as a clinical test for neurodegenerative disorders. 63 Recently NTP has shown particular promise for the early prediction of AD. 64 Importantly, NTP is related to tau pathobiology in connection with neurodegeneration, 63 and is thus likely to correlate with other tauopathies such as CTE. In addition to NTP, urine may also provide ready access for Ab measures. Complicating blood Ab assays is the interaction with predominant protein. However, normal renal filtration removes this confound, allowing smaller metabolites, possibly Ab peptides, to be detected more easily. The authors further suspect that smaller breakdown products of tau protein may be accessible in urine for the same reasons, which are readily detected by total-tau antibody. 65

Possession of the APoE-ε4 allele is a risk factor for dementia. 33 Carriers may have altered brain activity, even at a young age. 66 Long-term, but not short-term, effects of TBI may be influenced by APOE. APOE was not associated with poorer neuropsychological performance 1 month after mild or moderate TBI. 67 However, TBI was found to increase AD risk of APOE 10-fold 68 and cognitive decline after 30 years was greater in TBI patients with the APoE-ε4 allele compared with those without. 69 Environmental factors, in particular multiple concussions, may influence the effects of APOE. Boxers with the APoE-ε4 allele who had participated in many bouts were more likely to have CTE, while the allele was not a risk factor in boxers who had only experienced a few fights. 59

Certainly, more research is needed to better understand the chronic and catastrophic effects of repetitive head injuries.


United States

The National Center for Catastrophic Sports Injury Research in Chapel Hill, NC, reported 35 cases of SIS among American football players from 1980-1993. Seventeen were confirmed by necropsy, surgery, or magnetic resonance imaging (MRI) findings. Eighteen were probable cases of SIS, despite inconclusive necropsy findings.

The number of reported SIS cases increased from 1992-1998, but this increase is thought to be due to more frequent recognition and reporting. Some clinicians believe that SIS is overreported. Boden et al reported an average of 7.08 catastrophic head injuries per year in high school football, compared with 0.15 for college football from 1989-2002.1 The incidence was 0.67/100,000 for high school players and 0.21/100,000 for college players. Thirty-nine percent of the affected athletes reported playing with residual symptoms.1 There were eight fatalities, of which one individual had cerebral edema as the only radiographic finding. It was unclear as to whether a second impact occurred in this case.

With the advent and improvement of the helmet in American football and with the introduction of new rules that make spearing illegal, the incidence of head-injury fatalities has decreased from 2.64 cases per 100,000 persons in 1968 to 0.20 cases per 100,000 persons since 1977. The US Centers for Disease Control and Prevention estimates a 20% rate of concussion from football brain injuries (predominantly high-school and college level), which equates to an estimated 300,000 concussions per year.

Collins et al showed that 20% of the college football players they studied had two or more concussions during their career.7 Furthermore, a study by Daniel et al found that the symptoms of an estimated 60,000 football players who suffer concussion may persist for 4 or more months in up to 24% of these individuals.20

The US Consumer Product Safety Commission tracks product-related injuries through its National Injury Information Clearinghouse. According to the Consumer Product Safety Commission, an estimated 311,766 sports-related head injuries were treated at US hospital emergency departments in 2004.

Schulz et al reported on a prospective cohort study of North Carolina high-school athletes followed from 1996–1999.70 Subjects were clustered by school and sport, and the sample included 15,802 athletes, with 1–8 seasons of follow-up per athlete. Concussion rates ranged from 9.36 concussions per 100,000 athlete-exposures in cheerleading to 33.09 concussions per 100,000 athlete-exposures in football, where "athlete-exposure" is one athlete participating in one practice or game. The overall rate of concussion was 17.15 concussions per 100,000 athlete-exposures.

Cheerleading was the only sport for which the practice rate of concussions was greater than the game rate.70 Almost two thirds of cheerleading concussions involved two-level pyramids. Concussion rates were elevated for athletes with a history of concussion, and they increased with the increasing level of body contact permitted in the sport.

Powell and Barber-Foss reported a 2-year review of 235 US certified athletic high-school training records. The authors estimated a total of 62,816 cases of mild traumatic brain injury (TBI) annually among high-school varsity athletes, with football accounting for approximately 63% of these cases and a varied incidence among 10 other popular sports.71

Matser et al showed that 23% of the amateur soccer players they studied had 2-5 concussions during their career.16 Boden et al found that the overall prevalence of college soccer-related concussions was 0.6 cases per 1000 athlete-exposures for men and 0.4 cases per 1000 athlete-exposures for women.17 The authors reported that the vast majority (72%) of these concussions were grade 1, and none were grade 3.17

The actual number of athletes who may be affected by repeated minor head injuries is largely unknown.

Functional Anatomy

SIS is thought to occur because of a loss of autoregulation of the cerebral blood flow, which leads to vascular engorgement, increased intracranial pressure (ICP), and eventual herniation. This herniation may involve the medial temporal lobe and may occur medially across the falx cerebri or inferiorly through the tentorium. Herniation can also force the cerebellar tonsils to move inferiorly through the foramen magnum. The athlete's condition rapidly worsens, and brainstem failure occurs in 2-5 minutes.

Sport-Specific Biomechanics

The brain is protected by bone and is cushioned by tough meninges and cerebrospinal fluid. Despite these protective surroundings, blunt-force trauma to the head can cause injury to the site of impact (coup injury) and the site immediately opposite of the impact (contrecoup injury). Factors that dissipate the force (eg, equipment, neck muscle strength) can minimize this trauma.



The history is a key element in evaluating an athlete with a suspected head injury. However, the athlete may not be able to provide a good history because of slowed mentation or confusion. In such cases, obtain the history from a teammate, coach, or observer. Symptoms of a head injury may include the following:

  • Headache
  • Memory impairment
  • Confusion
  • Diplopia
  • Fatigue
  • Photophobia, phonophobia, or both
  • Blurred vision
  • Dizziness
  • Hemiplegia
  • Nausea
  • Sensory loss
  • Impairment of hand-eye coordination
  • Irritability
  • Depression


The goals of the physical evaluation are to (1) recognize that a head injury may have occurred, (2) determine which athletes require immediate transport to a medical facility, and (3) decide when the athlete can return to competition. Emergency management includes the ABCs of first aid. That is, assess and manage the individual's airway, breathing, and circulation. Signs of head injury include the following:

  • Altered levels of consciousness
  • Posttraumatic or retrograde amnesia
  • Gait abnormalities
  • Weakness
  • Visual abnormalities
  • Sensory loss
  • Pupillary concordance and/or accommodation
  • Poor concentration
  • Apprehension
  • Increased symptoms with exertion
  • Focal symptoms – Facial or extremity twitching, smelling of atypical odors, tasting of atypical tastes
  • Generalized symptoms – Tonic-clonic movements of body, incontinence, altered level of arousal

The brief neurologic examination should be performed without moving the athlete until the patient's ABCs and spine are deemed stable. The following are assessed:

  • Verbal quality and appropriateness
  • Memory (eg, to event), orientation (eg, to date), cognitive (eg, ability to perform the serial 7s test)
  • Visual findings – Pupillary size and reaction, tracking, nystagmus, gross visual fields, diplopia
  • Motor findings – Coordination (finger to nose), strength (focal findings), balance (eg, single-leg stance, heel to toe)
  • Romberg test results
  • Tone
  • Reflexes
  • Sensory abnormalities – Touch, pinch, and pain


Factors that may increase the risk of a poor outcome with a repetitive head injury include the following:

  • Previous head injury
  • Persistence of symptoms from a previous head injury
    • Headache
    • Labyrinthine dysfunction (balance disorder)
    • Visual, motor, or sensory changes
    • Mental difficulties that affect thought and memory processes
  • Alcohol or illicit drug use

Differential Diagnosis

  • Concussion
  • Facial Fractures
  • Facial Soft Tissue Injuries


Lab Studies

No laboratory tests help in diagnosing repetitive head injury. Most cases are diagnosed on the basis of the clinical findings.

Imaging Studies

Imaging studies are reserved for athletes with more significant injuries, such as those that cause loss of consciousness, persistent symptoms, neurologic deficits, or neurologic deterioration. Imaging studies should be considered in all athletes who have had more than 1 concussion. In addition, imaging studies should be ordered if symptoms last longer than 12 hours. Consultation with a neurosurgeon is imperative if any imaging findings are abnormal.

  • Plain skull radiography yields few findings in persons with mild brain trauma, and it should not be ordered unless facial fractures are suspected. Plain film radiography (cervical spine [C-spine] radiographs) can be ordered to rule out neck pathology, which can occur with head trauma.
  • Head computed tomography (CT) scanning is sensitive for detecting intracranial pathology associated with blunt-force trauma, even in a mild head injury (eg, Glasgow Coma Scale score of 13-15).
    • Nonenhanced CT scanning is the imaging examination of choice because acute hemorrhage must be excluded before performing contrast-enhanced CT scanning.
    • The advantages of CT scanning compared with MRI include (1) more rapid image acquisition in an emergency situation; (2) better depiction of bone; (3) lower cost, although cost should not influence clinical decision making in a potentially life-threatening situation such as the setting of a head injury; (4) correlation of negative results with a successful outcome; and (5) better sensitivity in detecting skull fractures.
    • Compared with the initial (first 12-24 h) head CT scan, the follow-up CT scan may better reveal small hemorrhages, which coalesce to form a brain contusion.
    • CT scanning can depict acute hemorrhages, skull fractures, cerebral edema, and cerebral herniation. An acute subdural hematoma is approximately 3 times more common than an epidural hematoma in sports-related head injuries.
  • MRI of the head is more sensitive than CT scanning for detecting subtle changes such as small hemorrhages, edema, and diffuse axonal injury (DAI).
    • MRI should not be ordered in emergency situations because CT scanning is faster than MRI and has the advantages listed above.
    • The advantages of MRI compared with CT scanning include the ability of MRI to better depict subtle edema, small hemorrhages, arteriovenous malformations, and DAI.
    • DAI is seen in severe head injuries and is thought to result from the shearing of multiple axons. DAI is represented on MRIs as diffuse, high-signal intensity specks in the white matter.
    • MRI should be ordered if the patient's symptoms persist and CT scanning results are normal or if the symptoms are atypical or worsen despite normal or stable CT scan findings.

Other Tests

  • Neuropsychologic testing
    • This is an in-depth examination of the injured athlete's thought processes and is considered the criterion standard for the initial and follow-up assessment of concussion patients, especially those with SIS.
    • A neuropsychologist certified by the American Board of Professional Psychology is the best resource for these assessments, and a consultative approach is preferred, as opposed to merely a description of test data.
    • A range of cognitive and behavioral tests are used, based on the preferences of the neuropsychologist, the severity of the injury, the specific clinical issue at hand (eg, return to school, return to work, manage finances), the educational and cultural background of the examinee, and the time post injury.
    • The occurrence of multiple concussions is associated with reduced cognitive performance on neuropsychologic tests.
    • Hinton-Bayre et al showed that impaired performance on psychometric tests continued even after the athletes (professional rugby players) were symptom free.72
  • Electroencephalography (EEG)
    • EEG yields conflicting and typically nonspecific results. Most of the research with EEG has involved boxers.
    • Busse and Silverman showed that 37% of abnormal EEG findings occurred in boxers who have had a concussion.73
    • Kaplan and Browder studied 1400 electroencephalograms in boxers and found that 34% of the athletes had normal EEG findings.27 The authors concluded that fighters with a lower ring rating had a higher percentage of disorganized EEG findings.
    • Johnson used EEG to evaluate retired professional boxers and found chronic brain damage in 12 of 15 of these individuals 22 years after their careers had ended.15
    • Other studies show abnormal EEG findings in 20-30% of boxers.
    • However, early studies by Beaussart and Beaussart-Boulenge did not find any correlation between EEG changes and the severity of postconcussion syndrome in 3100 cases.14
  • Dynamic imaging
    • Single-photon emission computed tomography (SPECT) scanning and positron emission tomography (PET) scanning have high sensitivity, but the specificity of these modalities is unclear and the clinical correlation is limited. At present, these tests are used primarily for research activities.
    • In addition, these examinations are expensive and not easily available to most clinicians.
    • Results from these tests may be overinterpreted or underinterpreted in medicolegal settings; the use for these types of activities should be discouraged until further definitive research is performed and has undergone peer review.


  • ICP monitoring may help in severe TBI, but it has limited usefulness in patients with mild TBI.
  • Patients with an ICP greater than 25 mm Hg generally have more unfavorable outcomes than those with lower ICP measurements.

Treatment & Management

Acute Phase

Rehabilitation Program

Physical Therapy

The goal of all therapy is to maximize the patient's strength and functional independence.

Athletes who have had severe head injuries may require rehabilitation for a prolonged period. In most patients, mild brain injuries do not require extensive rehabilitation, but they do require focal medical and rehabilitation care based on the individual's clinical evaluation and diagnostic test results.

Physical therapy is helpful in patients with increased tone, motor deficits, or mobility problems after a brain injury. Range-of-motion exercises are helpful in managing spasticity and preventing contractures.

Occupational Therapy

Occupational therapy is helpful in patients with brain injuries who may have motor and/or cognitive processing deficits and who may need to improve their ability to perform activities of daily living. The use of assistive devices can also be addressed.

Speech Therapy

Speech therapy is often useful in detecting subtle changes in the patient's thought processes and speech patterns. A speech therapist can help a patient with brain injury overcome barriers related to these changes.

Recreational Therapy

Recreational therapy is helpful in achieving community reintegration of the patient. Neuropsychologic measures may be good indicators of residual injury, and repeated testing may reveal when the athlete reaches a plateau.

Medical Issues/Complications

Medical issues in patients with brain injuries include the following:

  • Homeostatic abnormalities: Loss of autonomic control of blood pressure or respiration and cardiac abnormalities may occur.
  • Endocrine abnormalities: The syndrome of inappropriate antidiuretic hormone (SIADH) and diabetes insipidus are common problems.
  • Behavioral issues: The patient may become uninhibited, impulsive, or agitated. Aggressive treatment with behavioral programs, counseling, and short-term medication usage is most effective. Medication usage (mood stabilizers, atypical antipsychotics) should be instituted carefully and with full knowledge of the indicators of clinical success, duration of treatment, and potential adverse effects.
  • Deep venous thrombosis: Cifu et al showed that approximately 20% of patients admitted to a brain-injury rehabilitation unit had deep venous thrombosis.75
  • Pulmonary embolus: This is a rare condition, but if it is suspected, emergent treatment is indicated.
  • Complications of severe brain injury: Brainstem herniation, rebleeding, and death may occur.

Minor issues in patients with brain injuries include the following:

  • Dizziness: Most commonly, this is due to limitations in neck movement (pain) and peripheral trauma to the vestibular/labyrinthine system. Rarely, it is due to injury to the brainstem (central) balance coordinating structures. Dizziness is treated with medications and therapy.
  • Insomnia: This is commonly related to issues of pain, dizziness, behavioral problems, nightmares/flashbacks, altered physical activity levels, or idiopathic reasons. Insomnia is best treated with a rapid return to activity, treatment of secondary issues, and short-term nonaddictive sleep aides.
  • Behavioral issues: Behavior may vary from excessive (see above) or depressed. Normalizing sleep-wake cycles, controlling pain, reactivating physical skills, and reassurance help most individuals. Individualized psychotherapy is also highly effective.
  • Photophobia/hyperacusis: These conditions are rarely significant long-term issues. They should be treated aggressively initially with dark glasses/white-noise generators and then a rapid weaning program. Sustained difficulties may suggest an undetected injury or secondary psychologic issues.

Surgical Intervention

Evacuation is required for epidural hematomas, significant subdural hematomas, and large intracerebral hematomas that cause mass effect. Ventriculostomy may be required for significant edema and/or possible herniation.

Recovery Phase

Rehabilitation Program

Physical Therapy

In the case of a severe head injury, many of the aforementioned therapies can be continued in an outpatient setting, but most of the rehabilitation process is focused on reintegrating patients with brain injuries into their home environment and community.

Maintenance Phase

Rehabilitation Program

Physical Therapy

Patients with TBI may require educational or neuropsychologic support for an extended period, depending on the severity of the head injury.

Occupational Therapy

See Acute Phase, Rehabilitation Program, Occupational Therapy.

Speech Therapy

See Acute Phase, Rehabilitation Program, Speech Therapy.

Recreational Therapy

See Acute Phase, Rehabilitation Program, Recreational Therapy.


Care should be used when instituting therapy with medications that potentially have sedating effects, because sedation may complicate the monitoring of a patient with a brain injury. Some medications that can have significant sedating effects on such patients include H2 blockers (eg, ranitidine, famotidine), diphenhydramine, narcotic pain relievers, nonsteroidal anti-inflammatory drugs (NSAIDs), benzodiazepines, antipsychotics, and seizure medications.

Some medications may improve the patient's focus and alertness. A few of these medications are discussed below. In addition to the agents that may enhance thinking skills, aggressive management of specific symptoms is also warranted, including insomnia (trazodone), headaches (butalbital, aspirin, and caffeine [Fiorinal]; isometheptene mucate, dichloralphenazone, and acetaminophen [Midrin]; acetaminophen; NSAIDs; local agents), dizziness (meclizine, buspirone, vestibular programs, liberatory technique), and depression (cognitive behavioral therapy, selective serotonin reuptake inhibitors [SSRIs]).

CNS Stimulants

Class Summary: Central nervous system (CNS) stimulants are used to treat the hypoarousal and poor initiative often seen in patients with brain injuries.

Drug Name: Methylphenidate (Ritalin, Ritalin SR)
Description: Although most notably used in children with attention-deficit/hyperactivity disorder (ADHD), this agent often helps with hypoarousal. Frequently the first drug used in patients with brain injury.

Not used as often in children with brain injury; when used, administer as in children with ADHD.

Administered in morning and at noon before a therapy session to facilitate stimulant effect and increase attention to tasks. If no response is achieved, can be discontinued and another medication can be used.

Anti-Parkinson agents

Class Summary: Anti-Parkinson medications have been useful in patients with brain injuries because these drugs increase their arousal and attention to tasks.

Drug Name: Amantadine (Symmetrel)
Description: Unknown mechanism of action; may release dopamine from remaining dopaminergic terminals in patients with Parkinson disease or from other central sites. Less effective than levodopa in treating Parkinson disease; slightly more effective than anticholinergic agents.

Drug Name: Carbidopa/levodopa (Sinemet)
Description: May increase alertness and attention to task in patients with brain injury.

Central Nervous System Stimulant, Nonamphetamine

Class Summary: Nonamphetamine CNS agents have actions that are similar to sympathomimetic agents.
Drug Name: Modafinil (Provigil)
Description: May exert stimulant effects by decreasing GABA-mediated neurotransmission. Has wake-promoting actions similar to sympathomimetic agents. Improves wakefulness in patients with excessive daytime hypersomnolence. Has been used in narcolepsy and primary hypersomnia. Mechanism of action is unclear.


Return to Play

No good parameters have been proposed for repetitive head injury. As a result, most physicians use the parameters for concussion. The following systems present two options for concussion management, although many options are available. Note that in the following descriptions, asymptomatic means that the patient is symptom free at rest and with exertion.

Concussion Scales with Return-to-Play Criteria

Cantu system 76, 77, 78

  • Grade I – No loss of consciousness, or posttraumatic amnesia for less than 30 minutes
    • First concussion – Return to play if patient is asymptomatic for 1 week
    • Second concussion – Return to play if patient is asymptomatic for 2 weeks
    • Third concussion – Terminate season
  • Grade II – Loss of consciousness for less than 5 minutes, or posttraumatic amnesia for 30 minutes to 24 hours
    • First concussion – Return to play if patient is asymptomatic for 1 week
    • Second concussion – Return to play if, after at least 1 month, patient asymptomatic for 1 week
    • Third concussion – Terminate season
  • Grade III – Loss of consciousness for more than 5 minutes, or posttraumatic amnesia for longer than 24 hours
    • First concussion – Return to play if, after at least 1 month, patient asymptomatic for 1 week
    • Second concussion – Terminate season

Kelly system

The Kelly system grading is as follows:79

  • Grade I – No loss of consciousness, transient confusion for less than 15 minutes
    • First concussion – Return to play if patient is asymptomatic within 15 minutes
    • Second concussion in same contest – Remove from play
    • After fourth concussion in season – Terminate season
  • Grade II – No loss of consciousness, transient confusion for longer than 15 minutes
    • First concussion – Return to play if patient is asymptomatic for 1 week
    • Second concussion – Return to play if patient is asymptomatic for 2 weeks
    • Third concussion – Terminate season
  • Grade III – Loss of consciousness, brief (seconds) or prolonged (minutes)
    • First concussion with brief loss of consciousness – Return to play if patient is asymptomatic for 1 week
    • First concussion with prolonged loss of consciousness – Return to play if patient is asymptomatic for 2 weeks
    • Second concussion – Return to play if patient is asymptomatic for 1 month


The most common complication at follow-up is further head injury and/or cognitive decline. Matser et al found that concussion is specifically associated with impaired performance in memory and planning functions.16

A retrospective study of 31,272 children by Jimenez et al found that mental health utilization after a mild traumatic brain injury does increase in children without previous mental health disorders, however, 86% of the children who received postinjury mental health care had previous mental health disorders. 80


Equipment and rule changes have significantly reduced the number and severity of head injuries in American football over the last 25 years. The dramatic difference seen in football has sparked debate about equipment and rule changes in soccer because a significant number of concussions are now known to occur when players hit the ball with their head. A study by Stewart et al on 222 amateur soccer players found that intentional (heading) and unintentional head impacts are associated with moderate to very severe CNS symptoms such as dizziness and pain. 81, 82

In preventing SIS, the recognition of a concussion is the key factor. Preventing an athlete from returning to play while he or she still has symptoms from a concussion and following the guidelines for concussion management may help avert a catastrophic outcome.

The American Academy of Neurology (AAN) has issued a brief position statement on sports concussion. The AAN recommends caution and protection first: If an athlete is suspected of having a concussion or closed head injury, then first remove the athlete from practice or competition, and do not allow return to play until he or she is evaluated by a physician with experience in treating concussions and cleared for return.83


The prognosis varies with the severity of the injury. By definition, repetitive head injury is worse than a single minor concussion; neuropsychologic test results are worse in patients with repetitive minor concussions. Regarding SIS, rapid transport to a medical facility with neurosurgical specialists may prevent or limit the rapid decline often seen with SIS.


Educate athletes, coaches, and healthcare professionals about the potentially catastrophic effects of SIS. Coaches and healthcare professionals need to know how to prevent SIS by not allowing the athlete to return to play while he or she is still recovering from a previous head injury.


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Posted on BrainLine February 8, 2017. Reviewed July 25, 2018.

From Reprinted with permission.

Comments (31)

Please remember, we are not able to give medical or legal advice. If you have medical concerns, please consult your doctor. All posted comments are the views and opinions of the poster only.

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My loved one, a young adult in late 20s, has had multiple concussions. Though neurologists examined, no significant damage was seen on scans. HOWEVER, I am now seeing extreme lack of judgment and am getting worried. How do I approach this?

I've had at least 4 major concussions. I am also either always angry or depressed. Major mood swings. Chronic. Migraines. And multiple failed relationships. Denise age 53
So I've played hockey since I was 6, just some background, but useful in the sense of head trauma and sport. I received my first concussion at 15 years old, and another at 18. Since then I've fortunately managed to avoid head trauma and still play. Lately though my symptoms have been reappearing such as I'll get dizzy, nauseous and light sensitive out of no where. At one point was in the ER for spinal meningitis which came back negative. I've been on anti-inflammatory meds with no success, depression creeps in far too often which results in more anger/irritability. I know this will sound bad, and I wouldn't advocate breaking the law, but with that said after trying everything the only thing that has been consistently effective is marijuana, don't know why, don't really care because as anyone here with concussion history knows relief is all that matters when the symptoms are bad. I'm sorry if this isn't an option for many, but for those that can try I'd strongly urge since it's all that's worked for me. I'm also a whimp when it comes to pills so take that for what it's worth.
Travis, thanks for sharing your personal story
Thank you for that, Travis. I'm so so sorry you've been through this but how kind of strong of you to post

Hello everyone,

My name is Travis, I'm 36 years old and over the course of my preteen, teenage and early adult age I sustained 29 blows to my head including 10 diagnosed concussions. Most all of them took place when I was playing sports, and had a few accidents mixed in there also  About 3 years ago, I started noticing small changes at first, dizziness, a little confusion.  From then until now, the changes have become overwhelming.  Being angry all the time, confused, my short term memory is shot, and feeling depressed for really no reason at all.  I get confused with who I'm taking to, or what I'm talking about.  The doctors I've seen believe I have CTE, although it can't officially be diagnosed until after death.  To all those who have youngsters playing sports, please pay attention and watch them.  If they start having head injuries, you need to evaluate on if they should keep playing.  My mother watched all of the head trauma I had as a kid, and now I don't even remember talking to her or know who she is at times.  Thank you very much!


I'm a former hockey player who has had multiple concussions and now am seeing the effects at 47. I'm scared, can anyone help?

I was diagnosed with a Repetitive Head injury after many years of physical abuse from living with a brother with a violent temper.  My first concussion was at age one where I was hospitalized for several days and the head traumas kept coming.  Today I have also added on Post Concussion Syndrome to the list after my 19th concussion and worse fall happened this past Summer. I have scattered memories, frequent migraines, tremors, sensitive to light & sounds and get frustrated easily. 

I was hit by a car in traffic about a half year ago. I got a contusion. Doctors told me it would be a year until I could work again. But....after half a year I am feeling a okay. I can work fulltime.

Hello, I was abused as child and I'm 44 years old this month. I've had multiple head injury, concussions, and whiplash over the years. I struggled in school. I could study for test and know the material then couldn't remember a thing at the time of test. I was in a race car wreck where I broke the helmet when I hit my head on the door panel. A cop who likes to watch clocked me at 50 miles an hour at impact. I didn't get help right away. Next day went to E.R. didn't have health insurance. So was diagnosed with head injury, whiplash, concussion, chest and rib strain. I never got hospitalized or received help after returning home. I wasn't able to barely move,eat,or get out of bed for at least 2 weeks. I've always forgetful and hyper. From the child abuse, I've been told by siblings it has started as an infant. I've had severe migraines after I hit my head falling on ice at age 12. Friends say I was unconscious at least 5 mins. Never told my parents because of fear for the negligence on my part. My friends know a bit of the abuse but not the extent. So they never said a word for fear of me. I've been in multiple vehicle accidents (not at fault in any) where I suffered concussions and whiplash. On those occasions I only had e.r. visits when I was still in pain days later. Never received help after that. In 2010 my migraines got severe. I had no health insurance so I refused to be seen. I was in bed a month & 1/2. I was dehydrated severely, malnurished, and not able to function normally. Husband took me to the e.r. ( my fear also was I was given compizine in the e.r. once and nearly killed me. Put me in a comma for 4 days) E.R. stated it was normal for ppl whom were already almost unconscious from the migraine pain. By the 4th day my friend took me to a different hospital and was told I had a severe allergic reaction and if waited any longer to get help may have killed me) in 2010. The e.r. ruled out spinal meningitis. Was admitted for a week just to get the migraine under control. Was mostly in an unconscious state until the last night. Since I've been in different seizure meds and others. I've gain weight that I've been struggling to lose. The meds have increased other health issues I've had or may have been genetic. Some never struggled with till all the meds. But other family members have the same medical issues. (Not the concussions) over the course of this time, it's been bad. I've been receiving botox for close to a yr. I seem to be having improvements. Not so many E.r. visits. For a while it was everyday or couple x's a week. E.r. started to think I was there for the drugs themselves. Wouldn't believe me. I've had the same neurologist since 2010. One of the Dr's who saw me said I registered having a small brain. Seizure not seen from the outside. But now hospital claims to have no record of it. I've been tested about a yr ago for seizure migraines and tests came out ok. I take fioricet for the onstart of the migraines. And up to 3x's daily. Other then that it's ibprofen. I had a nervous breakdown in 2010 because of the migraines being everyday all day. They diagnosed me ADHD,bi-polar, PTSD, borderline personality disorder. And with anxiety and panic attack disorders. Those meds r also the cause of my weight gain which also lead to insecurity, self worthlessness, and depression. The Dr's wanna blame my migraines on stress and psycological behaviors. My phyco.therapist and psycologist keep stressing me claiming my health and migraines r caused from my stress, and anxiety. I can't get them to understand its the other way around. Even family and friends have agreed with me. Aug 10,2016 I was an another wreck kinda high impact. A guy Ran a yield sign speeding and I think on his phone. I tried to slam on my brakes N serve thinking he would do the same but him swerve left me right. I was headed north him East. He hit me on my driver side at my door and and front fender. Since he didn't see me til he was in the intersection,he hit me hard enough and me trying to stop and swerve the force of the hit pushed me head 1st into a telephone pole. I head my head on the door panel in the same area that I hit in the racecar wreck. The only difference is that the adjustment for tall and short ppl on the door panel was on my van. The racecar i have a 5seT harness. The adjustment on the panel rammed into the lower left side of my head. So by the time the ambulance got there, I already had 2 knots swelling up. I got whiplash from the side impact and head on impact. A post-concussion is what the e.r. called it. I hit my shoulder on the door pretty hard. My granddaughter was in the seat directly behind me. She's 5. If I hadn't if hit my brakes hard he would have hit her door and mine. I was in a mini van. He was in a full size Chevy extended cab pickup. I was so scared for her I wasn't thinking of myself. I knew I was hurt, but I always put myself last. We were seatbelt. I got the seatbelt strain across my chest and shoulder. At 1st no one would believe I was seat belted since I hit my head. But I was wearing a tank top and when paramedics examined me, they noticed when checking my shoulder injury that the seatbelt left abrasions on my shoulder. That help proved my case. I didn't go to the E.r. til the next night. I already owe 2 ambulance rides about $700 each. My ins. Doesn't cover them. So I didnt want another. After all my other 5 or 6 wrecks over the yrs I thought I would be ok. Then I didn't have a vehicle and my daughter was outta town so it wasn't til evening of the next day. I had a hard time getting them to believe me even though I had 2 huge welts on the left side of my head. And bruises on my chest. Oh when I went to swerve i guess I twisted my upper torso, so I had strained muscles on my left rib cage and left side of the back. I had severe motion sickness even while sitting or laying down. When going to stand the pain and dizziness was so bad my vision would black out out and I'd about pass out. I was off balance. I was barely outta bed for 3 weeks. I couldn't shower,dress,cook, or stuff like that without my husband's help. I barely made it off and on the toilet. Dr's had started me on physical therapy Oct6,2016. My ribs and chest were better by then mostly, my neck and head still was hard to move. And my left arm and shoulder. The next day Oct, 7th. After I got my son from school and was heading to get my granddaughter from school, my son and I got rear-ended in a low impact wreck. It reactivated it all again, except ribs and back. I already have back issues. My L3 &L4 have degenerative deterioration. I was back down again. Only new injury I had was I had pain down my left arm to my elbow, went by ambulance that time. I could barely move. In the ambulance that pain traveled to my fingers. In the e.r. I started having numbness and tingling in my left arm and fingers. I had left wrist and thumb pain. Being shoved forward jammed my shoulder to my wrist and thumb into the steering wheel. I had reached down to my cup holders with my right hand. So the force of impact was all on the left side. Since that shoulder was already injured, I wasn't holding the steering wheel with my full grip. Which was y the pain was down thru my wrist and thumb. I've been in physical therapy still. I've had a pain Dr for about 4or 5yrs now. I supposedly suffer from psycological chronic pain in my joints back, hands, and right knee. But the knee and low back I've proven deterioration. My pain Dr is the only 1 oh and the nurse practitioner who does my botox and most of my appointments for my neurologist. Believe I not only have some muscle damage from the yrs off abuse, but also nerve and joint damage. The other Dr's think it's in my head. E.r. has actually called me a hypochondriac and kicked me out once telling me they have done all they can for me for the migraines and don't come back. Was gonna give me pain shot and send me home. Instead gave me adivan thinking im just having a panic attack on top of things and sent me home. Never helped with pain, never checked, my eyes, or anything. I was in so much pain my blood pressure was in the 130's over 118 I think K was 1 of the highest for the diastolic. And my pulse was 115. When I left. My husband drove me over an hr away to K.U.Med center in Kansas City to their E.r. they helped me and kept me several hrs til they could reduce the pain which helped reduce my blood pressure to normal. I'm sorry got off track. Like I said before my 2nd wreck was 3 days shy of 2 months. I've been doing better, the numbness and tingling has gotten better in my left arm. E.r. wasn't worried about it. I'm getting better range of motion in my neck and shoulder. I still have issues but it's healing. Then last night I actually was cooking a good nice homemade dinner for my family for the 1st time in a while. Therapy has been doing a type of therapy with sports tape to strengthen the neck and shoulder muscles. The 2nd time within a few hrs my headache got severe. My neck wouldn't stop popping. (Which was very painfully when it did and would cause shooting pains in my neck and up my neck into the base of the skull. They had me remove it. Then we tried the tape again but lower.i was able to wear it almost a full week. Which is also good cause I'm allergic to alot of stuff. Then we tried again Wed or Thur. Fri 11 or 12th sorry I can't remember of Nov 2016 just day before, it started doing it again. I removed it. The migraine continued to increase, here it is 4:35 am and i still can't sleep cause of the pain. I'm half tempted to go to the e.r. but I hate being all drugged up then sleep it all off. The migraine is severe, but the nausea, vomiting, and dehydration is getting to me. I'm on Zofran but it's not helping. I see my pain Dr Mon. She does trigger point injections when I need them. Whether it's for my migraines (she will inject sections on my head,neck, and shoulders. She has even done injections under my eye brows. Because the pain behind the eyes.) The trigger point she uses for that r epidural injections to help ease it enough for me get under control. Since the botox I've not had to get as many injections for the migraines. Mon will be my 4th time to see her for the wrecks and pain. She has done injections the last 2of those. The 1st time I didn't have her do them because i had yet been able to get a follow up with my primary Dr or neurologist. Now I've gotta go again. I took the tape off, I've not gotten better. In fact my neck is popping a lot again. With the shooting pains, but now the dizziness is back, and blurred vision. Then the numbness and tingling is back in my arm. I'm scared to complain cause in afraid they would think I'm lying or just trying to squeeze money from those at fault. But I'm not. I know my pain dr will believe me cause all she has to do it start pushing my trigger spots and can tell when it's tight or bothers me bad. My last day of physical therapy is this week, and I'm scared cause I feel like I'm getting awful again. Please I need advice I was told in 2005 when I wrecked the race car that if I get very many more concussions it can be extremely serious. Since then I think this is my 3dr. I'm scared my memory is worse my psycologist took my off my Concerta and Ritalin because the pain has increased my blood pressure and pulse again. I've had pulmonary embolisms in the past and had a couple of other minor heart issues. So I'm a good candidate for a stroke. I'm upset because here in the last couple weeks my memory has gotten bad. I can't remember what I ate 2hrs before sometimes. My son gets upset cause I claim to never have seen a movie before and he says I have. I can watch it all over again and still not remember any of the scenes. I'm losing hope, but not ready to give in. Please, if anyone has advice and can comment please I'd greatly appreciate it. Oh by the way, tonight my migraine,dizziness, and shooting pain has been so bad my husband had to finish making dinner. Even the numbness & tingling has returned. Dr's tested me in the last yr for bi-polar tests, and ADHD tests to see if I am actually both. And a few months ago, I had to see a memory specialist. He said i do test as having quite a few neurons in my brain cells. Please I still have a lot of life ahead of me. I wanna be here for it, but also to enjoy it. Please scared to death to lose myself mentally and physically. I have too much to live for. Thank u and if u read all this thank u for taking the concerned time

I too had many concussions starting at quite an early age/6. At 11 I had my second. Soon after I began having seizures. My grades dropped dramatically. I hid my health from everyone but family. I had many concussions in high school from sports. I got drafted into the army. I again hid my health problems. Fast forward 3 years. Concussions again from sports, construction work, and accidents. All this time my brain is slowly getting screwed up. Then around 40 I'm diagnosed with MS. Keep a good eye out for many possible concussion side affects. They can be catastrophic!

I had my, I believe 9th, or 10th concussion about 2 years ago. Most of them were bad but my mum is a nurse, so I only had to got to the hospital once or twice. Ever since my last concussion, I"m just not right or all there. It takes me longer to understand what people are saying. My short term memory is absolute rubbish and my long term memory is kinda okay. My vision is progressively getting worse. I sleep maybe 16-18 hours a week, and that's if I'm having a good week. I never thought that maybe all those hits to the head might have had something to do with my current situation. If anyone has any kind of hyperlink to a website about long term effects caused by concussions it would be greatly appreciated. Thank y'all.

A few sports doctors are now trained in and are treating both internal and external head injuries which can result in concussion, mild to moderate to severe Traumatic Brain Injury. Very few doctors are trained to look for or treat invisible or Closed Head Injuries. Even neurologists, orthopedists, and ER doctors are not trained to look for, consider, or test for concussions or Closed Head Injuries. Even a severe Brain Injury will not show up on tests. A doctor specially trained in brain injuries is your best bet. Make sure to give them a list of your symptoms, the severity and how often they occur, plus number and type of injury incidents, Symptoms often include fatigue, headaches, nausea, balance problems, vertigo, insomnia, visions problems, etc. Symptoms can be very mild and eventually become chronic. Often people with concussions aren't even aware there is anything wrong. But symptoms will eventually appear. They can be behavioral changes like irritability, impatience, exasperation, depression, isolation, communications issues, poor judgment, sudden mood swings, and sudden bouts of anger or rage. Multiple incidents can lead to CTE (Chronic Traumatic Encephalography), where symptoms worsen Eventually leading to death. A simple slip and fall, or even falling and catching yourself can cause whiplash, internal concussion and Closed Head Injury. Keep a daily log of symptoms and issues. Rest completely until all symptoms are gone. The instant a symptom appears STOP and rest completely. NO computer or other electronic screens, NO TV, NO loud sounds, bright lights (especially florescents), and minimal gentle exercise until diagnosed. There is currently no diagnosis for CTE. If your symptoms are severe contact Boston University. Have someone research Brain Injury websites and print out phone numbers of doctors, hospitals who specialize in Brain Injury.

I was in a car accident about 14 years ago... I was in a intersection when a man in his eighties blew the red light, he was going about 55 mph... My head hit the window really hard and I was slammed around. I went to the hospital and was checked out... I now get shooting pain starting in my neck and up the whole side of my brain... I used to get it only once in a while and it didn't go up the whole side of my head, now it's all the time and painful when it does happen... Most of the time it's when I turn my head... I'm am also experiencing memory loss and sometimes confusion and can't go to sleep, I never knew all could be linked... Is this normal to have it start off as just once in awhile to having these systems all the time... It's been 14 years and I'm looking back and wondering if a lot of things that have occurred is because of this accident!

That sounds like a neck injury. Check out myofascial active release therapy to have that treated. It's referred pain from tight muscles caused by the accident.

I had tbi/pcs as a child and then more recently just getting better & have had more. Finding things very difficult & getting into rages, swearing etc. Need to keep stress to minimum not easy with tween alone. I scream & shout too much as she does. Gotta stop. House mess & will get no help. Cannot make decisions for life of me. Today talking & processing hard. Mindfulness, meditation, music, dance, mindful yoga, singing, swimming help. Lots on you tube etc. I feel there is a lesson in this for me as keeps happening?! Stop drinking, smoking etc, nutrition important too. Good luck.

I just left my boyfriend of 3yrs because of his fits of rage and abuse. He is 52 years old and has had over 10 concussions in his life, especially while surfing. These rages come out of nowhere, are very intense and violent, and illogical. I feel like the repeated concussions play a huge role in his behavior. Is there any help for this?

I hit my head in the back but the front hurts

My story and (Answers) to everyone. I was 7 when I almost died from my first concussion, 8 when the loud ring and ko came from a golf club, 9 from an abuse, and several after that I can't recall. Work i was always asked why didn't I do this or that, bosses would say process info, or they don't put up with stupidity. Being poor it drove me to work harder till I almost died from the stress and trying to please people. But now it seems as if good people are around, to help and challenge my thinking. I never knew how bad of a problem it was till I looked back. (ADVISE) FIND HOBBIES YOU ENJOY, AND STAY AROUND GOOD POSITIVE PEOPLE THAT WILL CHALLENGE YOUR THINKING. READ. Love life ( yolo) (to the smoker) stop I recently quit and it's helped me find other things to do and help get the gears turning. ( to the Mother) I had questions just like all I guess but all I got was idk or idk what to tell ya. All I can say to that is don't do that lol challenge and teach. Wish you all the best may God bless.

I played football in H.S. and College.  I've had many concusions. The last one i got I'm not sure if I was knocked out but my eyes crossed for 20 minutes.  I remember trying to get off the field and I was walking sideways.  I played the next week and every time I hit someone I would see a big white flash and then everything would go black for a few seconds.  I played the next game and the same thing would happen.  By the end of the game it looked like it was snowing but it wasn't.  Now I have memory loss, I can't remember high school at all.  I can't remember anything.  I get a headache every day.  I suffer from depression.  I have most of the symptoms on the list.  I don't know where to turn to and I'm really nervous about what the future will bring

i think it hurts and many people hate it but my brother had this and most of it is true. so believe everything

1st major tko 12yr old was out 20mins woke up sky was pink yellow some how still rode my bike home 30mins away brain swelled felt as if it was being cut out with a spoon 2nd 3rd 4th mini football loss of consciousness on all blurred vision when awoke lasting awhile.5th car accident tko started seeing spots then blind in middle of highschool next day vision returned then left side of body wemt numb on way to hospital. Then more through out college ball end result major deppression constantly drug resistant so far always exhausted these symptoms started shortly after 1tko and continued to get longer stronger as I aged my brain will be great to be studied long term affects of tkos

I suffered concussions during an assault. It has been five months.although the symptom has subsided.But I still don't feel very good. Mild Head ,fatigue and feel some weight on my mind and heart. Irritable also. What can i do?I really need some help.

I had a fall last July on the back of my head & then thd car knocked a speaker on me. I was knocked out for ages & suffering from pcs. Since had Knocks to head & had a woman accidentally knock me with a bag in the waiting room @ lost my temper & was all over the place. Am now worse again, moods, anger, headaches, noise. I lash out at my daughter which is not good & trying to get her to understand. Am very worried about more knocks to head. Wish everyone improvement- I practice mindfulness (helps), lots of baths, head forward, lavender oil, peppermint oil, fish oils.

Dear Sharon,

My friend went to a physical therapist recommended by her Neuro MD . the PT was able to get the crystals in her inner ear back in to the proper canals by using eye movement and gentle head manipulations..this helped her dizzy episodes.Apparently the concussion can cause the salt crystals to be dislodged and migrate in to the wrong canals which causes the nausea and dizziness. Best wishes with your healing.


I sustained many beatings as a child resulting in loss of consciousness and I know for a fact I also had many broken bones that never healed. I am in my 30's now and my life is a mess, i can't work, I have no friends, I have dysphagia, can't walk, am irritable, I light a cigarette and forget so I light another one, I can't do up buttons, I can't think properly I just wish I knew what was going on. Does anyone know the long term effects of repeated blows to the head in children?

I am so sorry to hear what you went through..(it happened to me too, almost daily.) The brain has an amazing ability to heal, and i wish you the best! Just reaching out to you because I also experience it and feel alone sometimes..Not many people have that kind of may consider speaking to your doctor about STEM Cell therapy. Some of my brain injuries have gotten better, though I still have epilepsy. Please tell me you have an advocate and a social worker?

Have you done any studies in children? My now four year-old hits his head frequently, probably a good blow once every-other-week. He is very prone to it. I have two other kids and they rarely do this. We are concerned about long-term effects. He has never lost consciousness. Any information would be helpful. We also plan on talking with our pediatrician.
I suffered from migraines for years due to perimenapausal symptoms. then in may of 2010 i sustained my first concussion. it was really terrible and i walked around not knowing a thing, what had happened, what i should do and so on. two days ago i sustained another blow to the head in the same place my first concussion/contusion was. i am very grateful for a website like brainline to help those who are left to find their own way through the dark. i can already tell this is going to be really bad. so i\'m praying
It has been a month, since I hit my head on the ice. I suffered the first concussion approx. 3 years ago. I still have dizziness,nausea,headaches,neck pain, loss of balance,focusing and sleep problems. When will these symptoms from the concussion go away. I had a CT scan and there was no bleeding, in which I'm grateful. The Dr. said I have a concussion. Should I go back to the Dr. or wait it out. I am not able to drive and I want my life to get back to NORMAL!!!!!!!!!!!!!!My family have been very helpful throughout this. If you have any ideas or information that might help me, I would appreciate it. Sharon