eMedicine Specialties > Psychiatry > Psychosomatic

Postconcussive Syndrome

Author: Roy H Lubit, MD, PhD, Assistant Clinical Professor, Mount Sinai School of Medicine; Clinical Faculty, Department of Child Psychiatry, New York University School of Medicine; Private Practice
Contributor Information and Disclosures

Updated: Oct 1, 2008

Introduction

Background

Traumatic brain injury can lead to deficits in 5 general areas: (1) short-term memory impairment, (2) slowed processing speed, (3) impaired executive function, (4) disrupted abilities of attention and concentration (which likely contributes to the deficits noted in the first 3 categories), and (5) emotional dysregulation.

Separating neurologically based symptoms from psychologically based symptoms such as posttraumatic stress disorder (PTSD) or adjustment disorder can be difficult.

DSM-IV-TR ¹ criteria outline for postconcussional disorder

A. A history of head trauma that has caused significant cerebral concussion.B. Evidence from neuropsychological testing or quantified cognitive assessment of difficulty in attention (concentrating, shifting focus of attention, performing simultaneous cognitive tasks), or memory (learning or recalling information).C. Three (or more) of the following occur shortly after the trauma and last at least 3 months:

1. Becoming fatigued easily2. Disordered sleep

3. Headache4. Vertigo or dizziness5. Irritability or aggression on little or no provocation6. Anxiety, depression, or affective lability7. Changes in personality (eg, social or sexual inappropriateness)8. Apathy or lack of spontaneity
D. The symptoms in criteria B and C have their onset following head trauma or else represent a substantial worsening of preexisting symptoms.E. The disturbance causes significant impairment in social or occupational functioning and represents a significant decline from a previous level of functioning. In school-aged children, the impairment may be manifested by a significant worsening in school or academic performance dating from the trauma.F. The symptoms do not meet criteria for dementia due to head trauma and are not better accounted for by another mental disorder (eg, amnestic disorder due to head trauma, personality change due to head trauma).

Second injury syndrome

The second injury syndrome (SIS), although rare, is important as a cause of preventable sudden death. SIS occurs when someone not yet fully recovered from a head injury experiences another head or upper body injury, even seemingly trivial injury. After a brief delay, the person suddenly loses consciousness. Signs of brainstem compression follow, leading to death or permanent coma. The syndrome typically affects young men who participate in rough sports. The mechanism may be failed cerebral autoregulation with subsequent engorgement of the brain vasculature.

Posttraumatic amnesia

Posttraumatic amnesia (PTA) describes the mental state of patients immediately following closed head injury (CHI) or after awakening from coma. PTA may persist for hours to weeks or, occasionally, months. Patients with PTA are alert and capable of complex behavior. However, they experience severe memory problems, feelings of confusion, inability to learn new information, and poor concentration. PTA sometimes involves peculiar alterations of consciousness and self-awareness. As a measure of injury severity, the duration of PTA has prognostic significance.

Posttraumatic thalamic syndrome

Injury to the thalamus following CHI produces posttraumatic thalamic syndrome. In this condition, the person progresses from generalized numbness to episodes of spontaneous pain or pain in response to nonnoxious stimuli. Patients also experience constant or episodic unpleasant sensations (burning, freezing, crushing, formication), paresthesias, outbursts of fear or anger, aphasia, abusive behavior, and signs of frontal lobe dysfunction.

Pathophysiology

The pathophysiology of postconcussive syndrome (PCS) results from contusions and diffuse axonal injury (DAI). Disruption of axons triggers a cascade of further insults, including calcium influx, excitotoxin release, phospholipase activation, and lipid peroxidation.

Postmortem studies of traumatic brain injury (TBI) have demonstrated pathological changes that cannot be detected by conventional neuroimaging studies. In fact, much of the pathology of TBI is under the threshold of detection in conventional MRI, which in humans is approved only to be done at 3 Tesla or less. Even when standard structural neuroimaging of the brain reveals no visible abnormality, underlying structural, biochemical, or electrophysiological abnormalities may be present.²

For example, Govindaraju et al examined volumetric proton spectroscopic imaging of the whole brain in mild TBI (mTBI) patients 1 month postinjury.³ This method provides a mechanism for detecting biochemical perturbations of the brain brought on by injury that would not necessarily show-up in standard imaging. The authors found “widespread metabolic changes following mTBI in regions that appear normal...” on conventional MRI. This supports the notion of nonspecific damaging effects from mTBI that occur at a subtle, microscopic level of injury⁴ and that one can have a significant brain injury, yet have normal conventional structural imaging. This has also been shown by Gaetz et al.⁵

Regarding pathophysiology, specifically of dementia after head injury, the pattern of symptoms reflects the nature of the injury and the location of tissue damage. Symptoms related to particular brain areas include the following:

• Prefrontal cortex - Disinhibition, apathy, personality change (coarsening, flattening), decreased fluency of speech, obsessions, hypochondria, delusions
• Basal ganglia - Depression, mania, tremor, cogwheeling, bradykinesia, obsessions, compulsions
• Thalamus - Apathy, irritability, pathological crying, paresthesias, pain, hypersomnia
• White matter - Apathy, lability, loss of spontaneity, transient hemiparesis or hemiplegia, bradykinesia, bradyphrenia
• Cerebellum/pons - Mild avolition, disinhibition, cerebellar signs, loss of ability to execute motor routines automatically

Frequency

United States

Persistent neuropsychiatric impairment following head injury is a significant public health problem. Military populations are especially prone to penetrating injuries, with relatively more closed head injuries occurring in civilian populations. From 400,000-500,000 people are hospitalized in the United States every year for head injury; many more people are injured and do not require admission. Head injury is the third most likely cause of dementia, after infection and alcoholism, in people younger than 50 years. The overall incidence of traumatic brain injury is roughly 200 cases per 100,000 population.

International

No information is available.

Mortality/Morbidity

Morbidity from closed head injury is variable and difficult to predict. Most estimates of morbidity stratify populations into those with mild, moderate, or severe injury, based on their scores on the Glasgow Coma Scale (GCS) and the duration of posttraumatic amnesia (PTA). By definition, mild injury entails less than 15 minutes of unconsciousness (GCS >13) or less than 1 hour of PTA in the absence of skull fracture. PTA of less than 1 hour predicts full recovery, while PTA of greater than 24 hours in adults predicts neuropsychiatric disability.

Between these benchmarks, the prognosis of an injury varies from complete recovery to persistent symptoms and disability. In 1968, a study by Lishman of 670 patients with either closed or penetrating head injuries yielded the following relationships between PTA and psychiatric disability or cognitive impairment.

Open table in new window

The numbers may have changed somewhat since 1968 due to improved survival and better means of assessment. Nevertheless, these data describe relationships that remain valid. Although severity of head injury as measured by depth of coma and length of PTA correlates with long-term sequelae, mild injuries sometimes lead to severe impairment and disability. Conversely, not all severe injuries have severe consequences. Other factors that predict morbidity include patient age, history of prior injury, history of alcohol use (especially at time of injury), history of psychiatric disorder prior to injury, location and extent of focal brain damage, degree of diffuse axonal injury (DAI), evidence of brain stem dysfunction at the time of injury, and psychosocial adversity before or following injury.

The factors related to injury severity correlate most strongly with problems of memory, cognitive slowing, and impaired information processing. They contribute to mood, personality, and behavioral sequelae to an immeasurable degree. Psychosocial adversity and stress also contribute to the morbidity of post–head injury dementia and of PCS.

Race

No relevant information is available.

Sex

Men experience head injuries more frequently than do women.

Age

Head injuries and their sequelae are most frequent in males aged 14-24 years. However, patients who are middle-aged or older are likely to have sequelae that are more persistent. Very young children with head injuries also have worse outcomes.

Clinical

History

Rapid improvement of head injury typically occurs within the first 6 months and often continues for 18 months. Problems continuing after 18 months usually continue indefinitely. Headache, dizziness, memory impairment, and fatigue are present in 30-50% of people during the first month after a mild head injury. In a prospective study of mild CHI conducted in Belfast, these symptoms disappeared within 6 months in 52% of cases and persisted in 16%. Of survivors, 32% reported a worsening of symptoms between 6 weeks and 6 months.

Significant functional impairment, marked by unemployment and marital dysfunction, typically accompanies PCS. In research populations, involvement in litigation plays a relatively small role in either the genesis or the resolution of patients' complaints.

• Patients treated for sequelae of head injury should be screened for the development or recurrence of any major psychiatric syndrome, with specific screening for the following:
  • Depression (See Medscape's Depression Resource Center.)
  • Anxiety
  • Mania
  • Psychosis
  • Obsessive-compulsive symptoms
  • Impulsivity
  • Suicide risk
  • Homicide risk: Because of their impulsivity and impatience, persons with head trauma can be combative to others, including family members and caregivers.
• Standard rating scales, especially the Hamilton Depression Rating Scale and the Positive and Negative Symptom Scales, are sometimes useful.
• Also inquire about subsyndromal complaints and nonspecific somatic distress, especially fatigue and headache. These, along with irritability, anxiety, apathy, and dysphoria, are cardinal features of PCS. Seizure phenomena, especially partial-complex seizures, should be explored specifically.
• The nature and severity of head trauma affect the nature and severity of sequelae. Obtain information from patients and usually from their hospital records about the injury, the immediate sequelae including unconsciousness and seizures, and the medical treatment received.
• Neuropsychological testing is the most sensitive means of characterizing the cognitive deficits of survivors of head injury.

Physical

Neurologic examination should include special attention to the following:

• Cranial nerves: Anosmia stems from damage to the olfactory tracts, confirming injury to the limbic system. Visual-field mapping may identify damage to the optic nerves. Nystagmus may reflect subtle labyrinth injury.
• Weakness: Hemiparesis may reflect diffuse axonal injury (DAI).
• Cerebellar signs include dysmetria and nystagmus.
• Signs of parkinsonism, including tremor, cogwheeling, and abnormal gait, confirm damage to the basal ganglia.
• Mental status examinations should be conducted repeatedly, with the date and time carefully noted, to follow changes over time. 
• Mental status:
  • Orientation: Patients with postconcussive syndrome may or may not be oriented to time and place. Disorientation is a very serious sign.
  • Appearance: Grooming and hygiene are usually intact, but in severe cases self-care declines.
  • Affect and mood: Depression, anxiety, labile mood, irritability or apathy may be present.
  • Speech: Fluidity may be impaired.
  • Concentration: Concentration is often significantly impaired.
  • Memory: Short-term memory and ability to learn new things is often impaired.  Remove memory is intact.
  • Psychomotor activity: Patients are often slowed up but could be agitated from lack of control and stress.
  • Energy: Patients are easily fatigued.
  • Sleep: Patients are often disordered.
  • Headache: Headache is often present.
  • Dizziness or vertigo: Dizziness or vertigo is often present.
  • Suicidal ideation: Suicidal ideation is a significant consideration in severe cases.
  • Homicidal ideation: Homicidal ideation is not typically associated with patients with postconcussive syndrome.
  • Delusions and hallucinations: Delusions and hallucinations are not part of the syndrome.
  • Comprehension: Comprehension may be impaired in severe cases.
  • Insight: Insight is variable.
  • Judgment: Patients with postconcussive syndrome may have impaired judgment from impaired cognitive abilities.

Causes

• Causes of head injury in civilian populations include the following:
  • Car accidents (50%)
  • Falls (21%)
  • Assault (12%)
  • Recreational activity (10%)
• Roughly 50% of these injuries are associated with alcohol use.
• In children, bicycle accidents are a significant cause of head injury, a clear indication for the need to wear a helmet when riding a bicycle.
• Among infants, most injuries reflect child abuse.
• Elderly patients are especially vulnerable to falls.
• Increased survival following severe injury contributes to the increasing overall number of people in need of treatment for late sequelae.

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