Postconcussional Disorder: Common result of head injury
Part 1: Introduction Etiology/Pathology
Postconcussional disorder encompasses a cluster of symptoms that frequently occur following mild traumatic brain injury. Recognizing the signs and symptoms is the first step in helping patients with their physical symptoms, cognitive deficits and emotional sequelae.
By Stephen D.Anderson, MD, FRCPC
Reprinted with the permission of the Canadian Journal of Diagnosis
Introduction
Postconcussional disorder (PCD) has been described in medical literature for over a century. The term post-concussional syndrome (now called PCD) was coined by Strauss and Savitsky in 1934.1 PCD is the most prevalent and controversial neuropsychiatric diagnosis following head injury. PCD is linked most commonly to minor head injury because it is not obscured by the myriad of findings that accompany a more severe brain injury. The constellation of symptoms includes physical symptoms, cognitive deficits and emotional sequelae (Table 1). PCD is actually seen in all degreed of traumatic-brain injury and should not be considered synonymous with minor head injury sequelae.
Minor head injury is a poorly defined term which refers to an injury to the head, face or neck area which does not necessarily cause injury to the brain. Minor head injury has often erroneously been used interchangeably with the term mild traumatic brain injury (MTBI). MTBI refers to a minor head injury in which there is also damage to the brain. MTBI is defined in Table 2; this definition includes:2
- The head being struck.
- The head striking an object.
- The brain undergoing an acceleration/deceleration movement (e.g., whiplash) without direct external trauma to the head.
MTBI with or without loss of consciousness can cause significant long-term brain damage as detected on neuropsychologic and positron-emission tomography (PET) assessments.3 The majority of studies, however, suggest that although PCD is seen in the vast majority of patients within the first month subsequent to MTBI, the prevalence of PCD is reduced significantly in the three to six months following the injury.4 Patients at high risk of having persistent PCD symptoms include those with prior history of head injury and the elderly. Psychologic factors may also influence late symptoms.
Etiology/Pathology
The human brain in particularly vulnerable to blunt head injury. Concussion can be reproduced only with great difficulty in primates and is practically impossible to reproduce in the smaller brains of other animals.5 For similar reasons, the cerebellum - which is much smaller than the cortex - is less likely to be affected by blunt head trauma. Brain damage caused by head injury is classified by whether distribution is focal or diffuse. Focal causes of brain damage include contusions and lacerations on the surface of the brain, bleeding deep within the brain (intracranial hematoma) and damage secondary to increasing intracranial pressure. Diffuse damage occurs with edema, shearing forces and hypoxic brain damage.
Alternatively, brain damage may be classified in terms of its distribution in relation to the damage force. Contusions and lacerations of the cortex occur either directly beneath the point of impact - the coup lesion - or at a distance, commonly on the opposite side of the brain, in the contre-coup distribution. Blows to the back of the head produce a contre-coup lesion in approximately 10% of cases.
PCD is presumably caused by rotational shear strains producing diffuse axonal injury. In a collision at high speed, the brain continues to move at thespeed of the vehicle before impact. Linear acceleration causes less damage than rotation because the incompressibility of the brain limits distortion. In contrast, because the brain has so little rigidity in its position in the cranium, rotation produces strain and distortion of its moorings; for example, a soccer player can strike a fast-moving ball with his or her head by taking care to avoid rotation of the head on impact. In contrast, an upwards and sideways blow to the chin of much less magnitude, by producing a rapid rotation of the head, may cause loss of consciousness or brain damage.
Studies on primates have confirmed that acceleration of the head without impact can cause severe diffuse destruction of brain substance.6 Even with impact at a variety of locations, however, the resultant contusions tend to appear on the undersurface of the temporal and frontal lobes and on the anterior pole of the temporal lobe due to contact with rough bony surfaces. Diffuse-axonal injury is invisible to the naked eye,is not usually detected with imaging techniques such as computerized tomography (CT) or magnetic-resonance imaging (MRI) and may even be unrecognized at postmortem unless microscopic histologic examination is undertaken.
Part 2: Features of Postconcussional Disorder
Features
The signs and symptoms of PCD may be physical, cognitive or emotional. PCD has been included in the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV).7
PCD is listed in the DSM-IV in a section that lists diagnoses which require further study. The essential feature, according to DSM-IV, is an acquired impairment in cognitive functioning, accompanied by specific neurobehavioural symptoms. The impairment occurs as a consequence of closed-head injury of sufficient severity to have produced a significant cerebral concussion.
Manifestations of PCD include loss of consciousness, post-traumatic amnesia and , less commonly, post-traumatic onset of seizures. There also must be documented cognitive deficits in either attention (e.g., concentration, shifting focus of attention, performing simultaneous cognitive tasks) or memory (e.g., learning of recalling information). Other symptoms that may occur include:
- Becoming fatigued easily.
- Disordered sleep.
- Headache.
- Vertigo or dizziness.
- Irritability or aggression with little or no provocation.
- Anxiety.
- Depression or affective ability.
- Apathy or lack of spontaneity.
- Other changes of personality (e.g., social or sexual inappropriateness).
The cognitive disturbances and somatic and behavioural symptoms develop after the head trauma has occurred, or represent a significant increase in pre-existing symptoms. The cognitive and neurobehavioural sequelae are accompanied by significant impairment in social or occupational functioning and represent a significant decline from a previous level of functioning.
Contrary to the DSM-IV definition, there are many reported cases of patients with long-term PCD symptoms who did not lose consciousness at the time of injury.8 Following MTBI, patients may have an impairment in their level of consciousness, but they may not have completely lost consciousness. Patients may also be able to move, talk and respond in a reasonable fashion and yet lack any insight into their actions or retain any memory of events around the time of injury.
Post-traumatic amnesia (PTA), an indicator of concussion which may lead to PCD, also needs to be adequately defined. The period of PTA is the interval between injury and the time when the patient begins to establish continuous memory of ongoing events. PTA includes the time during which the patient was awake but confused. Patients need to be carefully questioned. Approximately one-third of patients with traumatic brain injury give a history of an island of recall well before memories become continuous, resulting in a potential error in underestimating the total duration of PTA.9 The duration of PTA provides one of the best yardsticks of organic brain injury, correlating with the severity of diffuse brain damage and the overall degree of disability.10 Researchers have correlated the duration of PTA with the duration of time off work, the extent of neurologic disorder and associated physical disability, memory impairment and social and psychiatric disability
A more complete description of the physical symptoms, cognitive deficits and emotional sequelae of PCD follows.
Physical symptoms
- Headache pain is the most predominant physical symptom of PCD.
- Headache pain resulting from PCD may be extremely distressing and disabling.
- Vomiting, nausea, drowsiness and blurred vision are usually short-lived complaints. They are early symptoms which are experienced shortly following the head injury and are the typical complaints on the following morning. Headache pain and dizziness, however, may persist over time.
- Tinnitus may be disabling for some patients and may affect sleep.
- Diminished sense of smell may also be dangerous for patients if they are unable to smell smoke.
Cognitive deficits
The cognitive deficits of PCD are particularly disturbing for patients. A report from a neurosurgeon who experienced PCD following a minor sporting injury documents the handicap imposed by the subtle impairment of intellectual functioning.12 The neurosurgeon had difficulty remembering recent events, locating objects necessary for work, experienced problems with memory and the ability to concentrate on tasks. These symptoms persisted, but gradually improved over a period of 18 months. Family members frequently provide a history of the patient having memory difficulties, which may include:
- Difficulty organizing or processing information.
- Specific short-term memory deficits (e.g., verbal versus nonverbal).
- Trouble sustaining attention and easy fatiguability.
- Impaired selective attention and diminished ability to scan and shift information back and forth. Consequently, the patient frequently "gets lost" in group communication.
- Difficulties with initiation and planning of goal-directed activities.
- Impairment of abstract reasoning (e.g., the patient may interpret information literally and not symbolically, missing the true meaning).
- There may also be difficulty inhibiting action before action is required of after it should stop, resulting in impulsive and perseveration behavioural problems.
- Difficulty ordering or sequencing information.
- Difficulty learning from experience.
- Difficulty knowing when, where and how to ask for help.
Disorder of judgment and perception may cause misinterpretation of actions of intention of others. There may also be a tendency towards socially inappropriate verbal communication. Patients may also have an unrealistic appraisal of themselves and their strengths and weaknesses after brain injury. They often do not fully understand the nature of their deficits. Speed of information processing may also be slowed extremely, affecting reaction time and psychomotor activities (e.g., talking, writing, performing mechanical tasks). Patients may also be confused when presented with multiple bits of information at one time.
There may be communication disorders including overtalkativeness, disorder of thought and speech and inefficient word retrieval. Patients may use peculiar words and phrases and, in some cases patients may experience anomia or an uninhibited choice of words (e.g., four-letter superlatives). Patients are also extremely sensitive to the effects of lack of sleep, fatigue, stress, drugs and alcohol and their cognitive abilities will decline if these stressors occur.
Emotional sequelae
Numerous emotional sequelae occur with PCD. Common personality changes following brain injury include:
- Irritability.
- Impulsivity.
- Acting in socially inappropriate ways.
- Being unaware of one's personal impact on others.
- Being more emotional.
Emotional problems typically include poor tolerance for frustration, greater dependence on others, insensitivity to others and generally a more demanding attitude and increased helplessness. Emotional sequelae is understandable, given the areas of the brain which are most susceptible to damage following mild head injury. The frontal lobes are responsible for executive functioning, which includes the expression of language and speech, empathy with others, the ability to put aside immediate gratification, planning complex activities and the ability to anticipate the consequences of action. Damage to the frontal lobes may, therefore, cause a lack of foresight and insight as well as diminished control over impulsive and instinctive behaviour. In addition to emotional sequelae due to brain damage itself, secondary depression and anxiety may occur. Some patients may already be suffering from mild anxiety or depression that becomes exacerbated.13 Premorbid personality traits may also become exaggerated following MTBI. For example, a patient with premorbid perfectionist traits may develop an obsessive-compulsive disorder.
Part 3: Differential Diagnosis, Investigation, Management, Conclusion
By definition, PCD consists of symptoms which occur shortly following head injury. Differential diagnosis is, therefore, very limited. PCD must be distinguished from factitious disorder (the need to assume sick role) and malingering, in which the desire for compensation may lead to production or prolongation of symptoms. Post-traumatic stress disorder (PTSD) is rarely confused with PCD. PTSD symptoms includeintrusive recollections of the accident, avoidant behaviour and hyperarousal. 14 Patients may develop both disorders following major trauma, although concurrent PTSD is rare when amnesia for the trauma has occured. Patients may also develop symptoms due to temporal lobe epilepsy.
Investigation
Investigations may confirm organic impairment and help to reassure patients that they are not imagining their symptoms. Further investigations may be important to rule out other conditions and sequelae of closed head injury such as intracranial hematomas. Four main investigations following mild head injury include:
- Neurologic consultation.
- Imaging techniques.
- Neuropsychologic testing.
- Psychiatric consultation.
Referral to a neurologist is particularly relevant in patients who have cranial-nerve signs and symptoms, such as dizziness, tinnitus, hearing loss, diplopia and diminished taste and smell. In addition it may be appropriate to refer patients to an otolaryngologist or neuro-opthalmologist as indicated. Electronystagmography (ENG) may be helpful in assessing vestibular function. Electroencephalogram testing or brain-electrial activity mapping (BEAM) may be needed when temporal lobe epilepsy is suspected.
MRI reveals twice as many abnormalities in the brain as a CT scan following head injury.15 MRI has little diagnostic value, however, in cases of MTBI. Single-photon emission computerized tomography (SPECT) and PET have been used in investigating patients with PCD. PET scanning may demonstrate cerebral pathology not visualized by CT or MRI scanning and is particularly sensitive in identifying frontal lobe pathology.16 Findings of these functional-imaging techniques include abnormally-low uptake of glucose in presumable damaged areas.
For patients who complain of cognitive deficits, neuropsychologic testing is indicated. For many patients, imaging investigations and routine neurologic evaluations will be normal. Neuropsychologic testing helps to distinguish deficits that are directly related to the injury from those caused by depression and anxiety. Less commonly, testing helps to establish maingering or factitious disorder.
Neuropsychologic assessment tends to underestimate disorders and many valid problems are not registered on testing. Frontal-lobe deficits are difficult to detect with standard neuropsychologic tests; for example, subtle changes in attention and concentration, new learning ability, work retrieval and judgment often do not register. A negative examination cannot count as evidence against an organic cause of the patient's symptoms. Instead, careful interview of the patient and collateral information from friends and family may be more relevant. Testing patients within a few months of injury and repeat testing one year or more later can provide more useful information than a single examination. Repeat testing which reveals improvement indicates with a fair degree of certainty that the disorder began at the time of the head injury.17
Psychiatric consultation is indicated for patients who have a premorbid psychiatric history or who have developed major psychiatric illnesses (e.g., PTSD or major depression) or marked agitation following MTBI.
Management
Patients are frequently bewildered and overwhelmed by their symptoms. Despite having relatively mild injuries, they continue to be plagued by problems such as headaches, lack of energy, dizziness and an inability to concentrate or handle life's stressors. It is, therefore, not surprising that patients are frequently frustrated and angry. They require clear explanations from their physician regarding PCD and close follow-up of their symptoms. Patients with severe headaches may respond to a variety of treatment options, including ergot preparations, beta-blocker or antidepressants.18 Other symptoms, however, such as dizziness and vertigo, are highly resistant to therapy. Treatment of associated depression and anxiety is indicated. This may include antidepressant medication and/or supportive psychotherapy. Patients with anxiety symptoms may benefit from antidepressant medication or minor tranquilizers in addition to psychotherapy. It is important that patients who suffer from severe emotional sequelae be referred to a psychiatrist or a psychologist for ongoing treatment.
Rehabilitation specialists or psychologists who have expertise in dealing with head-injured patients may be of help with the cognitive deficits. Patients benefit from learning ways to optimize mental capacity, including time-management techniques. Pocket notebooks,, appointment books and watches with reminder alarms are helpful. Because these patients are particularly affected by stress and fatigue, it is important that they receive adequate rest (both physical and mental) and that they try to engage in important or difficult work during their periods of maximum competency.
Patients may need to reduce their work load, work on a part-time basis or leave work altogether until cognitive deficits improve. It is also important to refer patients, if possible, to specialized cognitive rehabilitation programs. Referral to a head-injury support group is helpful for family and relatives as well as for the patient. The use of a job coach may be indicated. Finally, due to the irritability and personality changes that may occur in PCD, marital therapy and/or family therapy may be indicated. Spouses often complain that patients are less attentive to them and, because of disorders of initiation and planning, patients are often seen as not caring or not being motivated to change their behaviour.
Conclusion
PCD encompasses a cluster of symptoms that frequently occur following MTBI. It is unnessary for a patient to have lost consciousness to develop PCD. Symptoms may be clustered into physical, cognitive and emotional sequelae. The most common physical symptoms are headache and dizziness. The most common cognitive deficits are disturbances in memory, attention and concentration. Emotionally, patients become irritable, fatigued and are prone to developing depression. In addition to routine investigation, careful questioning of collateral sources is important because patients frequently minimize their deficits. Patients require reassurance that they are not "going crazy" or that their problems are not "all in their head". PCD symptoms resolve in most patients within three to six months. There is a small percentage of patients, however, with persisting problems; possibly patients who have had a more significant injury or who have greater susceptibility to brain damage.
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