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Head Injury Follow-up

  • Author: David A Olson, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
 
Updated: Dec 22, 2014
 

Further Outpatient Care

This also depends on the degree of the head injury and the individual patient's cognitive and motor abilities and pain complaints.

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Further Inpatient Care

This needs to be individualized. Certainly after a moderate or severe head injury, transfer to an inpatient rehabilitation unit is recommended.

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Inpatient & Outpatient Medications

See Medical Care.

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Transfer

Patients with moderate or severe head injuries and head injuries with significant extracranial components are cared for best at a specialized trauma center.

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Deterrence/Prevention

See the list below:

  • Reducing morbidity and mortality rates associated with head injuries is likely to be difficult. Violence, automobiles, and drug and alcohol use are prevalent.
  • A study of community-based programs reported modest success, primarily by employing increased police surveillance and law enforcement to reduce overdrinking and alcohol-related injuries. Motor vehicle accidents in which the driver was intoxicated declined 6%, and more significantly, overall assault cases seen in local emergency departments decreased 42%.[123]
  • Another study has shown that patients who were screened for alcohol problems and provided with an organized intervention to reduce their alcohol consumption exhibited a 47% decrease in emergency department–evaluated injuries compared to patients receiving no alcohol screening or intervention.[124]
  • The use of protective devices also is promising. A meta-analysis of case-control studies of bicycle helmet use concluded that helmets reduce the risk of severe head and brain injuries by 63-88%.[125] Indeed, a 2006 study of 160 cyclist injuries in Singapore found that helmet users sustained head injuries only 5.9% of the time, compared with 40% of the time for nonusers.[126] Similarly, a California law mandating the use of bicycle helmets for riders aged 17 years and younger reduced traumatic brain injuries by 18%. However, subgroup analysis revealed that this reduction failed to apply to urban, female, and African American riders.[127]
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Complications

See the list below:

  • Mild head injury
    • Mild head injuries are those that generate GCS scores of 13-15. Such injuries usually are considered relatively benign, and the accompanying cognitive impairments typically resolve within 3 months of injury.
    • Patients with lingering complaints are often assumed to have either a psychological reaction to the injury or to be malingering. Various standardized neuropsychologic instruments are available to help sort out legitimate from illegitimate cognitive impairments. About 25% of patients with mild head injury taking such tests yield invalid profiles.[128] Furthermore, coexisting musculoskeletal injuries may impact cognitive testing. For example, collegiate athletes with musculoskeletal injuries performed just as poorly on computerized neuropsychological tests as athletes with concussions.[129]
    • However, an initial grading of mild does not necessarily mean a mild outcome. As many as 3% of patients with an initial mild injury may require a neurosurgical operation.[130] Some patients have died hours after sustaining trivial head injuries. Also, as previously mentioned, axonal damage has been documented pathologically with mild head injuries.
    • Disability rates may be pronounced with putatively mild injuries as well. Recent studies have demonstrated that following mild head injury, only 54-79% of patients are able to return to full preinjury employment. One study of 148 patients with mild head injury based on the GCS discovered that after 1 year, 26% had moderate disability and 3% had severe disability, but all these patients also had either radiological abnormalities or focal neurological signs, placing them in the more severe range of mild head injuries.[131] A recent review sponsored by the National Institute of Medicine concluded that there is no clear evidence of lasting cognitive impairments attributable to mild closed head injuries.[132]
  • Second impact syndrome
    • In the United States, athletic competitions account for 300,000 mild head injuries per year. The second impact syndrome occurs when an athlete suffers a minor concussion and subsequently is re-injured in play. The repeated concussive events are theorized to result in autoregulatory dysfunction and vascular congestion. Catastrophic brain edema, herniation, and sudden death may ensue.
    • At least 35 cases occurred among US football participants from 1980-1993, but the general incidence of this syndrome is unknown. Concerns about athletes at risk returning to play too soon have generated formalized recommendations from the American Academy of Neurology. Return to play is postponed for increasing lengths of time depending on the severity of the concussion.[133, 134]
    • Some researchers have questioned the existing literature's documentation of initial injuries, hypothesizing that the second impact syndrome is more one of primary impact and that secondary prevention strategies are not justified empirically.[135] Other researchers more recently have stressed the prolonged nature of recovery from athletic head injuries and the need for longer recuperation prior to return to play.[136]
  • Posttraumatic epilepsy
    • Posttraumatic seizures occur clinically in approximately 4% of patients with head injuries within the first week of the injury. Continuous EEG monitoring has disclosed a higher incidence (22%).[78]
    • Seizures after the first week occur in 4-30% of patients. The severity of the head injury, early seizures, depressed skull fractures, and temporal and frontal injuries identified on CT scans all have been associated with the development of late seizures.[137]
    • Although focal EEG findings traditionally have not been predictive of late seizures, one study reported that a focal EEG 1 month after injury resulted in a 3.49-times higher risk of posttraumatic epilepsy.[138]
    • Recently, MRI-visualized hippocampal sclerosis has been associated with intractable epilepsy in patients who sustained moderate-to-severe head injuries when aged 10-31 years.[139]
  • Posttraumatic headaches
    • Posttraumatic headaches are common and may occur in 30-90% of patients after a head injury.[140] The alterations in cations, catecholamines, and excitatory amino acids are similar in both migraine and head injury.[141]
    • Posttraumatic headaches typically manifest with a vascular component, but chronic daily headaches are also common.
    • Although controversial, some authors have reported that most posttraumatic headaches are primarily rebound or analgesic-overuse headaches. Nearly three fourths of such patients may benefit from cessation of pain medications.[142]
    • Greater occipital neuralgia can occur following head and neck injuries. Greater occipital nerve pain occurs in the back of the head and may be characterized by lancinating or aching sensations in this region.
  • Posttraumatic movement disorders
    • Tremor, dystonia, parkinsonism, myoclonus, and hemiballism all can occur following head injuries.
    • In a 2-year follow-up study of 398 patients with severe head injuries, 12% had persistent movement disorders. Disabling dystonia and low-frequency kinetic tremors were present in 5.4%. Parkinsonism and myoclonus attributable to the injury occurred in less than 1% of patients.[43]
  • Posttraumatic psychiatric disorders
    • Disorders of emotional functioning have been documented repeatedly after head injuries. A case-control study of 91 patients hospitalized with traumatic brain injury recorded a 33% incidence of major depression.[143] Depression has been associated with left frontal injuries. Bipolar disorder is also more frequent in patients with head injuries than in the general population and is associated with seizures and right hemispheric lesions.
    • Additionally, impulsive and disinhibited behaviors are common in patients with frontal injuries, although even obsessive-compulsive features have also been reported.[144]
    • Head injury-related psychosis is controversial. A case-control study of 45 patients with psychosis following head injury found that auditory hallucinations and paranoid delusions developed after a 54-month postinjury latent period. More widespread injury on neuroimaging and decreased cognitive functioning characterized the psychotic patients with head injuries compared with nonpsychotic control patients with head injuries.[145]
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Prognosis

See the list below:

  • This discussion has delineated a myriad of prognostic factors. Head injuries may result in death, a vegetative state, partial recovery, or full return to work. Each patient presents with a unique baseline neurological make up, mechanisms of injury, secondary complications, and postinjury adjustment and support system.
  • The most important prognostic factors are probably age, mechanism of injury, postresuscitation GCS score, postresuscitation pupillary reactivity, postresuscitation blood pressures, intracranial pressures, duration of posttraumatic amnesia or confusion, sitting balance, and intracranial pathology identified on neuroimaging.
  • The mortality rate of severe head injuries ranges from 25-36% in adults within the first 6 months after injury. Most deaths occur within the first 2 weeks.
    • A current study of 216 patients hospitalized during 2003-2005 in Ireland found 97% of patients with mild head injury attained a good recovery as measured by the Glasgow Outcome Scale, while 82% of the patients with severe head injury were either vegetative or markedly disabled. After 1 year, 11% of the total patients were unable to work.[146]
    • Another contemporary study of 309 Italian patients with moderate head injury found that only 15% were vegetative or severely disabled after 6 months. Basal skull fractures, subarachnoid hemorrhages, coagulopathies, subdurals, and poor emergency room clinical status predicted these unfavorable outcomes.[57]
    • Conversely, in Germany only 82% of 67 patients with mild or moderate head injury experienced a good 1-year outcome, and only 73% were able to return to work. Subjective complaints persisted in a large minority, with more than one third of patients reporting drowsiness, fatigue, forgetfulness, poor concentration, and irritability.[147] Other studies have identified dizziness along with analgesic and psychotropic medication use as predictors of failure to return to work after mild and moderate head injuries.[148]
  • An Australian study of patients with head injuries incurred from 1984-1991 found that all 59 patients who were aged 65 years or older and scored less than 11 on the postresuscitation GCS either died or were left with severe disability. Furthermore, even after controlling for injury severity and GCS scores, a current study of head-injured elderly motor vehicle accident victims demonstrated more than 3 times the mortality compared with their younger counterparts.[149] Future studies are needed to determine whether this grim prognostic indicator has more universal validity.[150]
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Patient Education

See the list below:

  • The physician may be hesitant to suggest to patients that problems may arise from a mild head injury. Such information may induce the expectations of symptoms when no symptoms are present and arouse anxiety. However, at least one study has shown that patients with head injury who were contacted by phone and offered education about their injury and follow-up care experienced significantly fewer postconcussive symptoms and less disruption of social activities.[151]
  • At present, most patients incurring a head injury probably should be informed that cognitive and emotional dysfunction as well as head pain and other somatic symptoms are not uncommon in the aftermath. At least in mild injuries, these symptoms typically are self-limited, and most people return to normal functioning after a few weeks to months.
  • For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center, Brain and Nervous System Center, and Eye and Vision Center. Also, see eMedicineHealth's patient education articles Concussion, Dementia in Head Injury, and Black Eye.
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Contributor Information and Disclosures
Author

David A Olson, MD Clinical Neurologist, Dekalb Neurology Group, Decatur, Georgia

David A Olson, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Florian P Thomas, MD, PhD, Drmed, MA, MS Director, National MS Society Multiple Sclerosis Center; Professor and Director, Clinical Research Unit, Department of Neurology, Adjunct Professor of Physical Therapy, Associate Professor, Institute for Molecular Virology, St Louis University School of Medicine; Editor-in-Chief, Journal of Spinal Cord Medicine

Florian P Thomas, MD, PhD, Drmed, MA, MS is a member of the following medical societies: Academy of Spinal Cord Injury Professionals, American Academy of Neurology, American Neurological Association, Consortium of Multiple Sclerosis Centers, National Multiple Sclerosis Society, Sigma Xi

Disclosure: Nothing to disclose.

Chief Editor

Stephen A Berman, MD, PhD, MBA Professor of Neurology, University of Central Florida College of Medicine

Stephen A Berman, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, Phi Beta Kappa

Disclosure: Nothing to disclose.

Additional Contributors

Joseph Carcione, Jr, DO, MBA Consultant in Neurology and Medical Acupuncture, Medical Management and Organizational Consulting, Central Westchester Neuromuscular Care, PC; Medical Director, Oxford Health Plans

Joseph Carcione, Jr, DO, MBA is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

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This 50-year-old woman with epilepsy seized and struck her head. Her initial Glasgow Coma Scale score was 12. Her scan shows prominent right temporal bleeding. She recovered to baseline without surgery.
This 50-year-old man was struck in the head in an assault. His scan shows a right acute subdural hematoma with no mass effect. His initial Glasgow Coma Scale score was 15. He returned home without major sequelae after 5 days of hospitalization.
This is a superior view of the CT scan shown in the previous image. This demonstrates a small left frontal intracranial contusion with some surrounding edema. This could be a marker of axonal injury.
This 23-year-old woman was in a motor vehicle accident with impact on the left. Her initial Glasgow Coma Scale score was 6 and she required intubation. Her scan shows a subtle right posterior frontal linear hyperdensity, most likely a small petechial bleed (contrecoup). This could also be a marker of axonal injury.
This 35-year-old man was in a motor vehicle accident. His initial Glasgow Coma Scale score was 7. He had left hemiparesis. He recovered orientation to temporal parameters after 1 week, but he remained disinhibited and hemiparetic (although able to ambulate). His MRI shows a diffusion-weighted hyperintensity in the right posterior internal capsular limb. This was attributed to an axonal injury. (An embolic workup for stroke was unremarkable, and no dissection was discerned on a carotid Doppler study.)
This 40-year-old woman was anticoagulated with warfarin (Coumadin) and fell out of her hospital bed. She subsequently died. Her CT scan shows an obvious right subdural hematoma with mass effect.
This elderly woman had a history of frequent falls and presented with seizures, possibly from her right hypodense subdural hematoma shown here. The subdural hematoma appears chronic and exhibits no mass effect.
This 23-year-old freelance graphic artist has drifted from job to job following his head injury 2 years prior to this scan. He was hospitalized initially for about 1 week for intracranial bleeding. This CT scan shows obvious medial bifrontal atrophy.
 
 
 
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