Articles

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.

Table 1: Symptoms of Postconcussional Disorder

	Physical Symptoms • Headaches • Nausea • Dizziness or Vertigo • Unsteadiness or poor coordination • Tinnitus • Hearing Loss • Blurred Vision • Diplopia • Convergence insufficiency • Light and noise sensitivity • Diminished taste and smell

	Cognitive Deficits • Memory (learning or recalling information • Attention and concentration • Initiation and planning of goal directed activities • Judgement and perception • Speed of information processing • Communication (aphasic and non aphasic) • Increased sensitivity to lack of sleep, fatigue, stress

	Emotional Symptoms • Emotional liability • Irritability, aggression • Personality change • Fatigue, decreased energy • Anxiety • Depression • Apathy • Disordered sleep • Loss of libido • Poor appetite

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.

Key Point

PCD is presumeably caused by rotational shear strains producing diffuse axonal injury. In a collision at high speed, the brain continues to move at the speed of the vehicle before impact.

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