Rhawn Gabriel Joseph, Ph.D.


Various definitions for what constitutes a "mild head" injury have been offered, many which differ in regard loss of consciousness, severity of injury, degree of memory loss, and so on (see Teasdale 1995, for related discussion). In consequence, the ability to accumulate reliable data on associated disturbances and recovery is therefore compromised. Moreover, as noted, many view mild head injuries as inconsequential when in fact that may not be the case (Kelly et al. 2013; Leininger et al. 2010; Miller 1993; Montgomery et al. 2013; Newton et al. 2014).

Moreover it is often erroneously assumed that consciousness must be lost in order for brain damage to occur. However, there is much evidence which indicates otherwise. In fact, as noted above, brain injury from shearing injuries (Adams et al. 1989), even in the absence of a head injury has been documented (Gennarelli 2016). In addition, what appears to be mild may be quite serious, even when CT scan and MRI fail to indicate brain damage (Newton et al. 2014). Indeed, some patients will die from a "mild" injury. On the other hand, the after-effects may also be quite insignificant.

In general, the period which encompasses "mild" for many investigators includes PTA and a loss of consciousness for up to 1 hour. However, even a loss of consciousness for less than 20 minutes can be quite serious, regardless of the extent of PTA.


Although an individual may suffer a concussion and memory loss without losing consciousness, concussion is characterized by a brief period of unconsciussness followed by an immediate return of consciousness. There are usually no focal neurological signs and the loss of consciousness is usually due to mechanical forces such as the blow to the head. As the magnitude of the applied force is increased the severity of the concussion increases.

Often immediately after an insult to the head the patient will drop motionless to the ground and there may be an arrest of respiration and an eventual fall in blood pressure (following a rise at impact)--death can occur from respiratory arrest. Vital signs usually return--even if the patient is unconscious--within a few seconds. Once respiration returns, the patient may begin to move about in a restless random fashion and may speak, usually unintelligibily. They may become abusive, irritable, shout, and resist contact.


As described in detail by Gennarelli (2016) there are two broad categories of concussion as well as distinct subtypes. These include mild concussion in which there is no loss of consciousness, and classic concussion which involves a short period of coma.


Mild concussion consists of several subtypes, these include focal concussion which is due to involvement of a localized region of the cerebral cortex. For example transient left sided weakness may be due to right motor involvement, whereas the patient who sees "stars" may have received an occipital injury. A diffuse concussion results in transient confusion and disorientation. In either instance these concussive injuries may or may not be accompanied by amnesia.

With greater impact, although the patient does not lose conscioussnes they may be confused, disoriented, and continue to motorically interact with their environment (Kelly et al. 2013; Yarnell & Lynch, 1970). That is, they may walk around and even speak to others. However, although immediate recall is intact, they later become amnesic for the event as well as the events leading up to the injury; i.e. anterograde and retrograde amnesia. The anterograde and retrograde amnesia may extend forward and backward in time for up to 20 minutes even without loss of consciousness (Yarnell & Lynch, 1970). When this occurs it is evident that they have suffered a significant insult to the brain.


Classic concussion is accompanied by a brief loss of consciousness at the instant of injury and is almost always associated with post traumatic amnesia. However, according to Gennarelli (2016), a patient with a classic concussion may remain unconscious for as long as 6 hours. If longer than six hours the patient has probably suffered diffuse axonal injuries such that large scale regions of the cerebrum have become partially disconnected.

In general, a mild (classic) concussion is associated with amnesia of less than one half hour, a moderate concussion with amnensia of 1-24 hours, and severe concussion with amnesia of 24 hours or more. Nevertheless, although the concussion may be considered mild, the accompanying brain damage may be minimal, moderate, or in a few rare cases severe.

In cases of classic concussion, immediately following the injury the patient develops apnea, hypertension, bradycardia, cardiac arrhythmias, and neurological disturbances such as decerebrate posturing and pupillary dilation. Thus the patient may seem temporarily paralyzed. Often, upon regaining consciousness they will vomit and complain of headache. Even in mild cases, there can result temporary alterations in the permability of the blood brain barrier, and damage involving the neuronal mitochondria.


A mild head injury is usually indicated by a GCS score of 13-15, no CT or radiological abnormalities, and a loss of consciousness for less than 20 minutes (some authors, however include those with unconsciousness lasting up to 1 hour, (e.g., Dikmen et al., 2016). This has also been referred to as cerebral concussion and patients need not have lost consciousness at the time of injury (Dikmen et al. 2013).

Although described as "mild" these injuries can be quite serious and involve various degrees of permanent brain damage. For example, anywhere from 1- 5% of those with mild head injuries may demonstate focal neurlogical deficits (Coloban et al. 2016; Rimel et al., 2011). In addition, 2-3% of those with mild injuries deteriorate after initially appearing alert and responsive (Dacey et al., 2016; Fisher et al., 2011). Moreover, 3% of those with mild head injury will develop increased intracranial pressure and life-threatening hematomas which must be removed (Dacey et al. 2016). Indeed, approximately 1 out 100 individuals with mild head injury die (Luerssen et al., 1988).

Brainstem Abnormalities.

It has been suggested that sheer-strain secondary to mild acceleration-deceleration injuries cause tearing of axons which is followed by degeneration of the neural tracts in the brainstem. Brain stem axonal degeneration has been experimentally demonstrated in monkeys with mild acceleration-deceleration induced injuries (Jane et al.1982), and among humans up to 40% of those with "mild" head injuries may demonstrate abnormal brain stem evoked potentials (Montgomery et al. 2013; Rowe, & Carlson, 1980). Similarly, those who have died from other causes demonstrate, microscopic neuronal damage, micro glial scars and fiber degeneration within the brainstem and cerebral hemispheres --even among those who received what was considered "trivial" injuries (Oppenheimer, 1968; Strich, 1969).

DAI & Contusions.

Diffuse axonal injuries (DAI) have been noted among those suffering brief period of unconscious (Teasdale & Mendelow, 1980). Moreover, contusions within the anterior temporal regions and frontal lobes have been found among those with mild non-impact concussions due to acceleration/deceleration injuries (Adams et al., 2011).


Individuals with mild head injuries have been repeatedly shown to suffer a variety of neuropsychological, psychosocial, and emotional impairments even in the absence of gross or focal neurological deficits. These include pervasive neurobehavioral impairments involving attention, memory, and rate of information processing. Patients may suffer word finding and expressive speech difficulties, reduced reaction time, perceptual-spatial disorders, and abnormalities involving abstract reasoning abilities. Moreover, although generalized recovery is often noted within 3 months of injury, a memory disturbances often remains and may in fact persist for years.

In some studies it has been reported that at 3 months post mild injury a significant number of individuals continue to demonstrate visual spatial abnormalities, memory disorders, reduced ability to concentrate, and persistent headaches, and as many as 34% of those with mild injuries may be unemployed at this time (Barth et al. 2013; Rimel et al., 2011). Interestingly, these deficits are not in any manner corrleated with length of unconscious or PTA, and in one study only 6 of over 400 patients were involved in litigation. Hence, purposeful malingering is not likely among the majority of such cases.


It is noteworthy that recovery appears to be dependent on previous mental abilities (Dikmen & Reitan, 1976; Miller 1993) such that the debilitating effects of mild head injury appear to effect individuals with minimal educational backgrounds more so than those with initially higher levels of functioning and education (Deb et al., 2009). This may be because these individuals have "bad brains" to begin with, and/or are less able to compensate for cognitive disturbances secondary to brain injury because of their more limited capabilities. That is, those with higher level abilities have more to draw from and to fall back on. Of course, they also have more to lose.


Following a mild (vs. severe or moderate) trauma to the head, patients may not begin to complain of cognitive disturbances until days or even weeks have passed (Alves et al. 2016; Miller 1993) even when consciousness has not been lost. Symptoms are often non-specific and are hard to quantify or objectively document. In general, these are referred to as post concussive disorders. Indeed, about 50% of those who suffer mild head injuries are at risk for developing post concussion symptoms (PCS).

PCS is manifested somewhat different for adults vs. children. Among adults, complaints regarding PCS may include persistent headaches, transient dizziness, nausea, impaired memory and attention, irritability, depression, anxiety, easy fatigueability, nystagmus, as well as inner ear disturbances such as vertigo, tinnitus, and hearing loss. Headache, dizziness, memory problems, weakness, nausea, and tinnitus are often the most common complaints--even at 12 months following injury (Alves et al., 2016; Zasler, 2009). Other symptoms may include hyperacoutism, photophobia, decreased judgement, loss of libido, and difficulty with self-restraint and inhibition.

In contrast, children often may become withdrawn, antisocial, aggressive, develop enuresis, as well as sleep disturbances. Moreover, it has also been reported that some individuals, children in particular, develop transient migraine-like attacks following even minimal injuries where consciousness was not necessarily lost (Haas & Lourie, 1988). These attacks include blurred, tunnel, and/or partial or complete loss of vision, paresthesias, dysphasia, confusion, agitation, headache, drowsiness, and vomiting --all of which come on like spells, particularly soon after the injury. It has been suggested that this is due to traumatic spasm of the larger cerebral arteries.

In general, post-concussion symptoms are varied in their degree and duration, although frequently they may persists for long time periods, from months to year or sometimes indefinitely (Dikmen & Reitan, 1976; Merskey & Woodforde, 2012; Miller 1993; Symonds, 2002). Nevertheless, even when PCS begins to wane it is sometimes followed by a long period of depression.


Many patients with PCS in fact develop a variety of emotional and personality difficulties which seem to be triggered by the experience of having had an injury (Bennett, 1969; Deb et al., 2009; Miller 1993). Patients may seem extremely anxious, fearful, depressed, and/or preoccupied with the details surrounding the accident, and remain (albeit periodically and transiently) upset for long time periods . Others may appear intolerant of noise, emotional excitement and crowds, and complain of tenseness, restlessness, inability to concentrate, and feelings of nervousness and fatigue. That is, they demonstrate the signs of post traumatic stress disorder. Many patients with this syndrome also seem unable to tolerate the effects of alcohol. The emotional disturbances may persist for months or years, but usually lessens as time passes.

It has been argued, and frequently it is suspected that PCS has in fact no objective basis and represents an exacerbation of pre-morbid personality characteristics or is motivated by a desire for financial compensation (Miller, 1961). Undoubtedly this is true in some cases. Nevertheless, frequently the majority of such individuals are not even involved in litigation (Barth et al., 2013; Merskey & Woodforde, 2012; Rimel et al., 2011). Moreover, sometimes the actual deficit is greater than the patient realizes (Prigatono et al. 2010; Waddell & Gronwall, 1984).

Cerebral Blood Flow.

Neuronal damage involving the brainstem and cerebral hemispheres as well as significant decrease in cerebral blood flow have been demonstrated among patients with mild and trivial head injuries (Montgomery et al, 2013; Taylor & Bell, 1966). In fact, many of these same patients were without PCS complaints and demonstrated normal circulation during the first 12 hours after their injuries and then within a period of 3 days developed post concussive symptoms and decreased cerebral blood circulation which lasted weeks and months. It has been suggested that this may be secondary to vasomotor abnormalities due to brainstem (medullary) impairment (Taylor & Bell, 1966).

Attention & Information Processing.

It has also been shown that patients with PCS and mild head injury are unable to process information at a normal rate (Gronwall & Writhson, 2014) and tend to become overwelmed. Frequently, however, patients do not complain about this until days or weeks later as this does not become apparent to them until they return to work and thus discover they are having problems. As such they may find that tasks which require attention to a number of details and which formerly were performed quite easily, now seem difficult and beyond their capacity. Hence, the patient says he cannot concentrate (Gronwall & Writhson, 2014; Miller 1993).

Presumably, many of the post-concussion symptoms are secondary to shearing forces associated with the acceleration/deceleration nature of their injuries as well as torque and other forces exerted on the brainstem. Indeed, following whiplash, patients may develop PCS, including vestibular symptoms and dizziness.

Whiplash & Blood Flow.

In whiplash the head is like a ball at the end of a whip and rapid or extreme rotations or extensions of the head may cause decreased blood flow by compressing the veterbral arteries which supply the brainstem, cerebellum, occipital lobe and hippocampal region of the temporal lobe (Chapter 33). This leads to symptomatic vestibular insufficiency and other brainstem responses (feeligns of giddiness, lightheadnesss, loss of balance), and can exert disrupting effects on memory and visual functioning. If the patient is suffering from atherosclerosis or abnormalities involving the cervical vertebrae (e.g. cerical osteoarthritis) the overall effects can become exacerbated even further.

Similarly, as is well known, the internal carotid artery is also very vulnerable to trauma, particularly in the neck where it is exposed. Hence, rapid extensions and rotations as well as karate-like blows, can tear and dissect the artery resulting in obstruction.

In general, tall persons suffer whiplash more often than shorter individuals, and those riding in the front of an auto are 50% more likely than those in the rear of sustaining such an injury (Elia, 2012). Slow speed crashes carry a greater chance of whiplash injury than high speed due presumably to patients becoming tense in realization of the impending accident.

As noted, acceleration/deceleration injuries are most likely to effect the brainstem, temporal and frontal lobe. In fact there is some suggestion that frontal injuries are more likely to give rise to postconcussional disturbances (Rabavilas & Scarpalezos, 2011). However, brainstem and temporal lobe abnormalities are obviously contributory. Vertigo, Hearing Loss & Tinnitus.

Damage to the inner ear (which is situated within the temporal bone) is frequently associated with the development of vertigo, dizziness, and tinnitus. As noted, the temporal bone (which contains the auditory meatus) is often subject to injury, including fracture regardless of where the head was initially struck. Hence, the presence of vertigo and tinnitus following a head injury suggest a concussion of the ear ear (Elia, 2012).

Some patients also complain of hearing loss or even unilateral deafness. In some cases this is secondary to an injury of the tympanic membrane, external auditory canal, or the inner skin of the ear. This results in some bleeding and thus the potential development of dried blood clots (and cerumen) in the auditory canal which subsequently plug the ear reducing auditory acuity by impeding sound transmission. In addition, in cases of temporal bone fracture, cerebrospinal fluid may escape into the ear thus temporarily disrupting functioning.

On the otherhand, some patients complain of increased sound sensitivity. It has been proposed that this is secondary to rotational acceleration forces which stretch and cause traction of the stapedius muscle which is attached to the vestibule and stapes of the ear.

Diploplia & Photophobia.

It has been proposed that visual problems such as diplopia may occur secondary to traction of the eye muscles. That is, the eyes may almost pop out of the socket, or they may actually pop out of the socket, which of course would put considerable strain on the optic nerve. If the oculomotor nerve is injured in any manner, this too may cause diplopia and may also contribute to the development of nystagmus (Elia, 2012). Nystagmus usually resolves over time.

Photophobia and excessive sensitivity to light may also be secondary to occulomotor traction. Interestingly, it has been demonstrated that many such patients with minor head injury are consequently more sensitive than they realize (Waddell & Gronwall, 1984), and some demonstate a hypersensivitiy to both sound and light when in fact this was not a complaint.

PCS & Severe Head Injury.

It has been noted that those with mild injuries sometimes complain of PCS more so than those with severe injuries (Levin et al., 2017). This in turn has led to the unfounded suspicion that these disturbances have no objective basis. However, in some cases as patients recover and progress from severe to moderate or moderate to mild degrees of disability, they begin to make these same complaints. Moreover, there is some possibility that due to the greater degree of cognitive and personality disorganization among those with severe injuries that their ability to appreciate and complain of these disturbances is lessened (i.e. lack of insight, decreased motiation). In this regard, frequently patients with severe brain injuries do not become or demonstrate depression until after there has been considerable recovery (Merskey & Woodforde, 2012).


Individuals who sustain repeated head injuries sometimes have a history of emotional, impulse, and educational difficulties. Some individuals suffer head injuries because of reduced functional capabilities and thus place themselves in dangerous situations, drive recklessly, and so on. In fact it has been reported that as many as 50% of head injured individuals have a history of poor premorbid academic performance, including learning disabilities, school drop out, multiple failed subjects, as well as social difficulties (Fahy et al. 1967; Fuld & Isher, 1977; Haas et al. 2017; Miller 1993).

The finding that many head, and even spinal injured patients (Morris, Roth & Davidoff, 2016) have also suffered previous cerebral traumas has led some investigators to suggest that these individuals have a life style which seems to predispose them to violence and injuries to the cranium (Tobis et al., 1982). As suggested by Haas et al., (2017), this relationship may be due to poor attention span, distractability, limited frustation tolerance, poor judgement, impulsivity, difficulty anticipating consequences, perceptual-motor abnormalities, etc. all of which makes these individuals more susceptible for being involved in an auto accident. However, it is also possible that once someone has a head injury, due to subsequent decreases in overall functional efficiency, that they are less likely to avoid situations where a second (or third) injury may occur.

Life style and premorbid social-emotional stability are in fact important contributors to the possibility of suffering a head trauma. For example, chronic alcoholics are especially susceptible to cerebral injury (Bennett, 1969; Miller 1993). It has also been reported many head injured patients have suffered a bout of depression or other emotional disturbances (e.g. fight with a girlfriend) immediately prior to their injury (Tobis et al. 1982).

Overall, the individuals most at risk for suffering a head injury at some point in time are young males (Teasdale 1995), particularly those with a history of learning disability, alcohol abuse, social-emotional difficulties, and previous head trauma. Indeed, males are twice as likely to suffer head injuries as females and also more likely than females to engage in "risky" and "macho" behaviors, which of course puts them at the greatest risk. Conversely, it is also males who are more likely to downplay the significance of their injury and who will display the most resistance to rehabilitation, and in particular, psychotherapy.


Copyright: 1996, 2000, 2010, 2018 - Rhawn Joseph, Ph.D.