Postconcussion syndrome (PCS) refers to nonspecific neurologic, cognitive, and psychologic symptoms that result from traumatic brain injury (TBI) and persist beyond the expected recovery period. Concussion is an acute trauma-induced alteration of mental function lasting <24 hr, with or without preceding loss of consciousness. Approximately 90% of concussion symptoms resolve within 10 to 14 days, but some may linger.¹ The extent and severity of lingering symptoms are highly dependent on the testing and reporting used. PCS can also follow moderate and severe brain injury, although it is more commonly associated with mild brain injury or concussion often without loss of consciousness.

PCS

Postconcussive syndrome

Posttraumatic nervous instability or brain injury

Postcontusion syndrome or encephalopathy

Status post commotio cerebri

• Incidence is approximately 27 cases per 100,000 persons/yr.
• From 30% to 80% of patients with mild to moderate brain injury will experience some symptoms of PCS though this is variable.¹
• Risk factors for prolonged symptoms include children, female sex, low socioeconomic status, anxiety sensitivity, previous TBI, severe bodily injury from TBI, headaches, and unsettled litigation.²
• Recurrent TBI, especially when symptoms of previous injuries still exist, significantly increases the risk and severity of future postconcussive syndrome.
• Acute postinjury symptoms such as headache, dizziness, photophobia, diplopia, or tinnitus are associated with development of persistent symptoms.¹

• Symptoms start within a few days to weeks after the head injury and usually persist after 3 mo; 15% of patients or more will have persistent symptoms 1 yr later.²
• At least three of the following symptoms after TBI are required to meet ICD-10 criteria:
  1. Headache (usually of frontooccipital location and showing characteristics of tension or migraine headache)-occurring in 25% to 78% of persons after mild TBI.
  2. Fatigue.
  3. Dizziness and/or vertigo-occurring in approximately 50%. Associated with risk for prolonged recovery.
  4. Impaired memory.
  5. Difficulty in concentrating.
  6. Insomnia-occurring in approximately 33% acutely and 25% more chronically.
  7. Irritability/frustration.
  8. Lowered tolerance of stress, emotion, or alcohol.
• Other associated symptoms: Noise sensitivity, neck pain, nondermatomal paresthesias, interference with social role functioning.
• Detailed neurologic exam focusing on orthostatic intolerance, cognitive function, vestibular function, extraocular movements, gait, balance, and coordination. Abnormalities are often subtle.^3,4
• May need to test for impaired saccades or vestibulo-ocular reflex abnormalities, cervical motion abnormalities, and impairment on tandem gait forward and backward.⁴

• The inciting TBI may occur as a result of events such as falls, motor vehicle accidents, military injuries, and contact sports.
• The primary injury triggers a slew of pathophysiological changes at the cellular level secondary to the axonal stretching and injury, leading to alterations in membrane and intracellular physiology, thereby affecting neurotransmission. These changes are believed to be a factor in determining whether the outcome will be an apparent normal recovery or persistent postconcussion symptoms.
• Postmortem findings reveal diffuse axonal injury as the primary pathologic finding, along with small petechial hemorrhages and local edema.
• Prior history of anxiety is a strong risk factor for occurrence of PCS.

• Headache (dissection of the vertebral artery, occipital neuralgia)
• Epidural hematoma
• Subdural hematoma
• Skull fracture
• Cervical spine disk disease
• Whiplash
• Cerebrovascular accident
• Benign paroxysmal positional vertigo-common after head injury
• Depression
• Anxiety
• Posttraumatic stress disorder

• Neuropsychologic testing, which often reveals difficulties in concentration, memory, language, and executive function
• To exclude other causes of neurologic symptoms after TBI:
  1. Normal results of electroencephalography
  2. Normal evoked potentials

Various biomarkers in blood and cerebrospinal fluid and genetic testing have been proposed and studied in patients with TBI, but these tests are not specific and are not routinely used in clinical practice.

Chronically, if not improving, consider growth factor and other neuroendocrine markers.⁵

• There is no imaging modality to diagnose PCS. PCS is primarily a clinical diagnosis. The American College of Emergency Physicians’ clinical policy regarding neuroimaging in adults with mild traumatic brain injury is summarized in Box 1.
• 10% of computed tomography (CT) scans of the head following mild TBI are abnormal, showing mild subarachnoid hemorrhage, subdural hemorrhage, or contusions.^1,2
• MRI of the head after a mild traumatic brain injury (mTBI) is abnormal in 30% of patients with normal CT scans and may show irregular brain contours or old cerebral contusions.
• More advanced imaging modalities, including diffuse tensor imaging (DTI) and susceptibility weighted imaging (SWI) in MRI, functional MRI (fMRI), and metabolic imaging such as magnetic resonance spectroscopy (MRS), positron emission tomography (PET), and single-photon emission computed tomography (SPECT) imaging, can show acute and chronic changes even after one mTBI, although they have not found a major role in clinical practice yet.³
• None of the imaging modalities have been able to predict the occurrence of PCS in patients with mild TBI.³

• Early reassurance and patient education are major components of treatment. Explanation of symptoms and expectations, combined with early follow-up with reassurance, may hasten resolution of symptoms.
• Early and graduated physical activity is preferred over prolonged cognitive and physical rest. Light aerobic activity that avoids risk for reinjury has been shown beneficial in mitigating refractory concussion symptoms. Physical and occupational therapy may be beneficial.³
• Cognitive behavioral therapy may be effective in treating symptoms.
• Avoidance of alcohol, narcotics, and sleep deprivation.

• Supportive symptomatic care may include the use of nonnarcotic analgesics and antiemetics.
• Amitriptyline has been widely used for posttraumatic tension-type headaches as well as for nonspecific symptoms such as irritability, dizziness, insomnia, and depression.² Amantadine is also a consideration.
• Posttraumatic migraine-type headaches can be treated with a trial of propranolol or amitriptyline alone or in combination.
• Depression can be treated with selective serotonin reuptake inhibitors but may not respond as well when compared with patients without PCS who have depression.
• If symptoms are not improving, consider testing for hypopituitarism since complete or partial hypopituitarism (most commonly growth factor) can be a sequelae of mild TBI and has overlapping symptoms with postconcussion syndrome.⁵

• Most patients improve after mild TBI without any residual deficits within 3 mo, though the cognitive and emotional symptoms resolve more slowly.
• Although good improvement is typically seen within the first 6 mo, patients can continue to show improvement for up to 12 to 18 mo.
• Patients with very severe brain injuries (low Glasgow Coma Scale [GCS] score) and prolonged anterograde amnesia are at increased risk of development of some degree of permanent cognitive and personality disturbance.
• Predictors for the development of persistent PCS include:
  1. Female sex
  2. Ongoing litigation (conflicting studies)
  3. Low socioeconomic status
  4. Prior headaches
  5. Prior TBI
  6. Prior psychiatric illnesses, particularly anxiety

Early consultations with psychologists, psychiatrists, neurologists, and rehabilitation specialists in an outpatient setting may be beneficial.

Postconcussion Syndrome (Patient Information)

Concussion (Related Key Topic)

Traumatic Brain Injury (Related Key Topic)