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Treating Arthritis with Prescription Medication Living with a chronic disease such as arthritis can be intimidating. Understanding Arthritis The first step to coping well with arthritis is to understand what you can about it. MMTR Physiotherapy will Present Research at ACRM Conference October 7th to 11th 2014 marks the 91st ACRM Conference. On TV and in movies, heroes, villains, and innocent bystanders, are often knocked upon the head, rendering them temporarily unconscious, after which they awake, good as new. Traumatic brain injury may well be as common as stroke as a leading cause of neurological injury and death in America and Europe .
The number of individuals who suffer significant head injuries is actually unknown, and is open to debate, as not all those who suffer head injuries, including even those suffering loss of consciousness, seek treatment.
Unfortunately, some physicians and emergency room personnel also down play the significance of "mild" head injuries, particularly when the patient appears to have more immediate and life threatening problems.
Lying above the pia matter is yet another very thin web-like fibrous membrain referred to as the arachnoid.
Sitting above the leptomeninges and partially adhering to the inside of the skull is a thick, tough, leathery-like membrain, the dura mater (i.e.
The dura not only acts as a hard shield protecting the brain from the skull but forms a number of compartments which partly encompass and support various portions of the cerebrum. Although seemingly smooth on the outside, the skull is not completely smooth and rounded on the inside as it consists of several small bony protrusions and cavities. If the skull is struck by a blunt object, the impact area will flatten with stress oscillating outwards laterally --like a rock hitting a pool of water. Basilar fractures often extend into the base of the skull and are difficult to detect unless quite severe.
In some instances these fractures may extend in an anterior, posterior or lateral direction.
If extending laterally they may damage the mastoid bone and tympanic membrane of the inner ear resulting in dizziness and disturbances involving equilibrium. Basilar fractures are sometimes associated with tearing of the dura as well as CSF leakage. Usually with depressed fractures, part of the skull will shatter into several fragments which are driven downward toward the brain.
The outer surface of the brain is covered by the dura and meninges, and the various compartments of the brain such as the cerebral hemispheres are separated by a tough leather-like material such as the falx cerebri. Frequently, but not always, the meningeal artery may be torn and intracerebral, extracerebral or an epidural hematomas may develop. When the head is struck there usually results an inward deformation of the skull immediately beneath the site of impact whereas the surrounding area is bent outward. Linear fractures involving the temporal-parietal bones may damage the auditory meatus, eustachian tube, and ear drum causing hearing loss, tinnitus, disorders of equilibrium and vertigo. In some instances, longitudinal fractures may damage the cochlear nucleus and cause injuries to the 7th and 5th cranial nerves which pass through this area before innervating the skin and muscles of the face. Anosmia (loss of the sense of smell) and an apparent loss of taste (loss of aromatic flavor perception) are frequent sequalae of head injury, especially following injuries to the face and fractures involving the back of the head or frontal bone. The cribiform plate is a wafer thin sheet of perforated bone through which the olfactory nerves pass on their journey from the nasal mucosa to the olfactory bulbs. With damage to the olfactory nerve and cribiform plate, sometimes there also may result a laceration or rupture of the meninges, If there is meningeal rupture cerebrospinal fluid will leak into the nose.
Fractures near the sphenoid bone (which juts out beneath and below the frontal bone within the skull) may result in laceration of the optic nerve. In some cases an individual may be struck so hard that their eyes pop out of their sockets. 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 2004, for related discussion). Moreover it is often erroneously assumed that consciousness must be lost in order for brain damage to occur. In general, the period which encompasses "mild" for many investigators includes PTA and a loss of consciousness for up to 1 hour. Although an individual may suffer a concussion and memory loss without losing consciousness, concussion is characterized by a brief period of unconsciousness followed by an immediate return of consciousness. 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. As described in detail by Gennarelli (2006) there are two broad categories of concussion as well as distinct subtypes. Mild concussion consists of several subtypes, these include focal concussion which is due to involvement of a localized region of the cerebral cortex. With greater impact, although the patient does not lose consciousnesw they may be confused, disoriented, and continue to motorically interact with their environment (Kelly et al. Classic concussion is accompanied by a brief loss of consciousness at the instant of injury and is almost always associated with post traumatic amnesia. In general, a mild (classic) concussion is associated with amnesia of less than one half hour, a moderate concussion with amensia of 1-24 hours, and severe concussion with amnesia of 24 hours or more. 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. Although described as "mild" these injuries can be quite serious and involve various degrees of permanent brain damage.
In general, mild degrees of hypoxia are associated with dizziness, confusion, blurring of vision or difficulty seeing in the dark, whereas, moderate degrees produce loss of vision, nausea, coma and amnesia (Morgan & Gibson, 1991; Sokoloff, 1981). Characterisically, following head trauma there is an immediate and global reduction in cardiac output and blood flow for a few seconds, which in turn results in oxygen deprivation. Unfortunately a vicious deteriorative feedback cycle can be produced by these conditions which further reduces the brains supply of blood and oxygen.
With respiratory distress, hypotension, and hypoxia, there results pulmonary hypoperfusion and an increase in blood platelets in the capillaries.
Frequently, particularly with severe head injuries, the vasacular system may be traumatized due to shearing and stretching of the blood vessels. Head trauma can also result in secondary cardiovascular abnormalities including myocardial damage.
It is important to note, that even with a minor head injury, if there is an injury to the chest (i.e. Hence, a variety of conditions associated with head injury can conspire to produce widespread hypoxia and disturbances involving cerebral metabolism.
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. Diffuse axonal injuries (DAI) have been noted among those suffering brief period of unconscious (Teasdale & Mendelow, 1980). 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.
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. 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. 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.
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). 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, 1991; Taylor & Bell, 1966). It has also been shown that patients with PCS and mild head injury are unable to process information at a normal rate (Gronwall & Writhson, 1974) and tend to become over welmed. 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).
Similarly, as is well known, the internal carotid artery is also very vulnerable to trauma, particularly in the neck where it is exposed.
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, 1972). Damage to the inner ear (which is situated within the temporal bone) is frequently associated with the development of vertigo, dizziness, and tinnitus.
It has been proposed that visual problems such as diplopia may occur secondary to traction of the eye muscles. Photophobia and excessive sensitivity to light may also be secondary to oculomotor traction.
It has been noted that those with mild injuries sometimes complain of PCS more so than those with severe injuries (Levin et al., 1987). Individuals who sustain repeated head injuries sometimes have a history of emotional, impulse, and educational difficulties.
The finding that many head, and even spinal injured patients (Morris, Roth & Davidoff, 2006) 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). Life style and premorbid social-emotional stability are in fact important contributors to the possibility of suffering a head trauma. Overall, the individuals most at risk for suffering a head injury at some point in time are young males (Teasdale 2004), particularly those with a history of learning disability, alcohol abuse, social-emotional difficulties, and previous head trauma. Following a blow to the head the skull will bend inward and sometimes strike the brain causing a contusion directly below the site of impact, i.e. Contusions and bruises are usually found in the orbital frontal regions and anterior and lateral temporal lobes bilaterally as well as along the convexity regardless of where the skull was struck (Adams et al., 1980). In general, contusion may consist of multliple hemorrhages which develop immediately upon impact along the crests of the various cerebral gyri. When the brain has been contused, severely compressed, or subjected to rotational shearing forces, axons are often severed and cells crushed. Trauma to the brain may interfere in axonal transport in otherwise normal neurons (see Burke et al.

When consciousness is not lost following a head injury it is frequently erroneously assumed that the brain was not damaged. Contre coup contusions are usually associated with translational linear acceleration injuries and the free movement of the head. As pertaining to coup and contre coup lesions, rapid increases in acceleration sometimes cause the development of increased intracranial pressure at the trauma point, and decreased (contre coup) pressure at the opposite side of the cerebrum.
In contrast, impact to the front of the skull almost always results in frontal lobe (coup) injuries. In certain types of head injuries, such as those involving a great deal of force and movement the brain will swirl, rotate, oscillate, and slosh around inside the skull in a rotary fashion. Nevertheless, as the brain swirls about the neocortical surface becomes contused, sliced and sheared by the the bony protrusions (e.g. However, rotational acceleration and decelerations injuries can create extensive subcortical and brainstem damage as well.
For example, when subject to severe rotational forces there sometimes is tearing at the pontine-medullary junctions (where the brainstem meets the midbrain), such that in consequence the brainstem is partly torn loose and disconnected from the rest of the brain (Hardman, 1979; Jennett & Plum, 1972).
In addition to contusions, rotational injuries are associated with venous tears, arterial shearing stresses, and hemorrhagic lesions in the midline region and throughout the brain. When axons are severed or stretched the capacity to transmit electrical-chemical impulses and thus transmit information is attenuated.
In general, DAI takes the form of axonal retraction balls in those who die within days, microglial scars in those who live days to weeks, as well as degeneration of the fiber tracts among those who survive for longer time periods, e.g. Frequently brainstem, midbrain, and thalamic damage are secondary to acceleration rotational forces.
Nevertheless, in these later instances the patient may seem normal for some time after the accident. Loss of consciousness sometime after the injury is not always due to the development of hemorrhage. Following a head injury, with or without skull fracture, the arteries and veins running above, below, or through the meningeal membranes (which cover the brain) may be stretched, broken, pierced, or ruptured. Epidural hematomas are also not very common as they tend to occur in less than 10% of all patients with severe head injury. Subdural hematomas are the most common of all and are associated with a very poor prognosis. Acute and chronic subdural hematoma may be unilateral or bilateral with an onset latency period of days or weeks. Hematomas are potentially life threatening and can cause extensive brain injury, including prolonged coma, the development of vegetative states, and even death. As pressure continues to develop the midbrain and diencephalon are shoved down into the posterior fossa compressing the brainstem. In general, the ability to obey simple commands is often considered as indicative of the return of consciousness. One need not actually suffer a severe head trauma in order to sustain significant damage to the brain and cognitive loss. Nevertheless, it does appear that when a patient has lost consciousness, the longer the period of unconsciousness, the more widespread and debilitating is the injury and the loss of cognitive capability including memory functioning.
Two general indicators of severity are length of unconsciousness and extent of memory loss, both retrograde and anterograde (i.e. The GCS is composed of three major categories, Eye Opening, Motor Response, Verbal Response.
There is also a significantly high mortality rate for individuals who remain in a coma for 6 hours or more (Jennett et al., 1977). In addition, the longer the coma the worse are the prospects for rehabilitation and the greater is the long term disability. The majority of patients who die, however, when first seen are often in a state of shock with subnormal blood pressure, hypothermia, fast pulse, and pale-moist skin. Some patients will remain in a coma for months or even years and never regain consciousness.
After a few weeks these patients may open their eyes, first in response to pain, and then later spontaneously.. Indeed, in one case a vegatative patient was misdiagnosed as oriented to person (although she could not communicate) simply because sometimes she would open her eyes and seemingly fixate (for 1-3 seconds) on people who made sounds or called her name. Nevertheless, among those is a vegetative state there is wakefulness without awareness and the patient remains inattentive and never speaks or gives any consistent sign indicating cognition or awareness of inner need. It has been argued that the term "persistent" should not be applied until at least 1 year has elapsed since injury (Berrol, 2006). This can lead to longer lasting symptoms called Post Concussion Syndrome or Traumatic Brain Injury or simply TBI. These are complex sets of neuropsychological disorders with symptoms lasting weeks, months or even years after the initial injury.
TBI patients complain mostly about problems with their memory, mood and ability to concentrate. But in reality, a knock upon the head sufficient to render loss of consciousness typically also causes brain damage. Well over a million individuals a years seek medical attention in the United States alone, and 500,000 require hospitalization, with 70,000 developing long term disabilities, and 2,000 remaining in persistent vegetative states. Moreover, children who are abused and beat seldom come to attention of authorities or medical personnel unless their injuries are life threatening or exceedingly obvious. Basilar fracture are relatively uncommon whereas approximately 75% are linear, the remainder being depressed. Laceration and contusions are usually found beneath the broken bone fragments, and subdural hematomas may develop on the contralateral side (Bakay et al., 1980). However, it has been reported that patients with linear fractures who retain consciousness are 400 times more likely to develop a mass lesion (e.g. Indeed, the temporal portion of the skull may fracture following trauma to any portion of the cranium. In others, although the eyes do not pop out, their main be strain on the optic nerves thus causing visual problems and light sensitivity.
However, even a loss of consciousness for less than 20 minutes can be quite serious, regardless of the extent of PTA. 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.
These include mild concussion in which there is no loss of consciousness, and classic concussion which involves a short period of coma. 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.
Nevertheless, although the concussion may be considered mild, the accompanying brain damage may be minimal, moderate, or in a few rare cases severe. For example, anywhere from 1- 5% of those with mild head injuries may demonstrate focal neurological deficits (Coloban et al.
This is followed by a transient hypertension and then a prolonged hypotension (Crockard et al. For example, hypoxia induces vasodilation and constriction of the blood vessels, a condition which results in intracranial hypertension. Unfortunately, the increased number of blood platelets actually act to obstruct the blood vessels thus further reducing blood flow.
Moreover, the blow itself or the action of rotational forces can cause vascular spasms of the carotid arteries as well as the anterior and middle cerebral arteries (Bakay et al, 1980). For example, if the brainstem medulla has been compromised, there may be abnormal activation of the vagus nerve which influences heart rate, the result being atrial fibrillations--a condition which in turn sometimes results in stroke. 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. These include pervasive neurobehavioral impairments involving attention, memory, and rate of information processing. 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).
Nevertheless, even when PCS begins to wane it is sometimes followed by a long period of depression. 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. Indeed, following whiplash, patients may develop PCS, including vestibular symptoms and dizziness.
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, the temporal bone (which contains the auditory meatus) is often subject to injury, including fracture regardless of where the head was initially struck. In some cases this is secondary to an injury of the tympanic membrane, external auditory canal, or the inner skin of the ear.
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.
It has been demonstrated that many such patients with minor head injury are consequently more sensitive than they realize (Waddell & Gronwall, 2004), and some demonstrate a hypersensitivity to both sound and light when in fact this was not a complaint. This in turn has led to the unfounded suspicion that these disturbances have no objective basis.
Some individuals suffer head injuries because of reduced functional capabilities and thus place themselves in dangerous situations, drive recklessly, and so on.
As suggested by Haas et al., (1987), this relationship may be due to poor attention span, distractibility, limited frustation tolerance, poor judgement, impulsivity, difficulty anticipating consequences, perceptual-motor abnormalities, etc. For example, chronic alcoholics are especially prone to cerebral injury (Bennett, 1969; Miller 1993).
This results in cell death (necrosis) within the first 24 hours after injury --a process which may continue for up to a week. However, a patient may in fact suffer significant cognitive disturbances and extensive contusions and lacerations throughout the brain even with no loss of consciousness.
Indeed, the fact that the frontal and temporal regions are most severely effected regardless of, as does the findings that when there is a skull fracture, contusion are maximal on the side of impact. This can occur at the moment of impact or if the head is suddenly subject to rapid changes in motion (such as when the patient is air borne after been thrown through the windshield of their car vs.

Because the cerebral hemispheres sit atop the thin brainstem, there can result torque in the pontine-midbrain junction thus disconnecting these lower from higher regions. Nevertheless, the degree and type of damage which occurs is dependent on the speed, and direction at which the head moves.
If severe, there can result a permanent loss of functional capability accompanied by an immediate and prolonged loss of consciousness.
These brain structures may also be damaged as a consequence of intracranial hemorrhage, ischemia, compression and herniation.
However, as blood continues to leak and the brain becomes increasingly compressed, within a few hours or even days the patient begins to complain of headache, drowsiness, and confusion. Most are secondary to fractures of the temporal-parietal area and laceration of the middle meningeal artery. Upon waking they seem lucid, but then as the hematoma develops they begin to increasingly complain of headache, irritability, confusion. These hematomas develop following damage to the various veins criss-crossing the subdural space. Hence, although an initial CT-scan may have been normal, if a patient subsequently deteriorates, the possibility of hematoma should be entertained. Because of its compartmental arrangement, pressure may be high in one region of the brain and less so in yet another. Pressure developing from a mass lesion tends to displace the brain and in particular the cerebellum in a downward direction This also results in brainstem compression as the cerebellum is forced down in the foramen magnum.. Hence, a patient in a vegetative coma and completely unresponsive would receive a score of "3", whereas an individual who is fully responsive and alert would receive a score of "15". Based on a review of a number of reports it appears that patients with a GCS score of 8 or less have a mortality rate of approximately 40% (35-50%), and that as the scores decrease the death rate increases. Similarly, among children intellectual deficits and academic difficulties becomes more severe as coma length increases.
Supposedly children suffer a lower risk of mortality from head injury as compared to adults. For example, those over 40 with severe injuries have a death rate of up to 70% whereas the mortaility rate for those below forty is 23% (Nikas, 1987). They may grimmice, flex the limbs or blink to threat or to loud sounds and may make roving movements of the eyes. For most people, they appear seven to 10 days after a concussion and last up to three months. It is the injury to the brain which induces the unconscious state, and the longer the unconscious period, the greater is the damage to the brain.
Almost half of such injuries are due to falls (especially in children and older adults), with assault, automobile accidents, gunshot and stab wounds comprising the bulk of the remainder.
In addition, men with supposedly "mild" head injuries, tend to downplay the significance of their injuries and are often reluctant to seek medical attention unless cognitive and physical functioning is significantly compromised.
The dura mater is richly innervated by blood vessels, including the middle meningeal artery (which is sometimes subject to laceration following skull fractures creating a epidural hemorrhage). This is a serious concern as anywhere from 50-70% of those with severe head trauma are hypoxic following injury (Klauber et al., 1985).
With decreased respiration there is decreased reoxygenation of the blood all of which favor the development of hypotension and hypoxia (Staller, 1987). For example, due to pulmonary edema or lung shunting, the ability of the lungs to transport oxygen to the blood is reduced (systemic hypoxia). Patients may suffer word finding and expressive speech difficulties, reduced reaction time, perceptual-spatial disorders, and abnormalities involving abstract reasoning abilities. Interestingly, these deficits are not in any manner correleated with length of unconscious or PTA, and in one study only 6 of over 400 patients were involved in litigation. Others may appear intolerant of noise, emotional excitement and crowds, and complain of tenseness, restlessness, inability to concentrate, and feelings of nervousness and fatigue. 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 presence of vertigo and tinnitus following a head injury suggest a concussion of the ear ear (Elia, 1972).
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.
In fact it has been reported that as many as 50% of head injured indivduals have a history of poor premorbid academic performance, including learning disabiities, school drop out, multiple failed subjects, as well as social difficulties (Fahy et al.
When this occurs there may be a buildup of neurotoxics which in turn result in cell death throughout the neuroaxis. Rather, it has been postulated that much of the damage which occurs secondary to impact or non-impact (including coup and contre coup) injuries are due to the effects of rotational acceleration and shearing forces. When this occurs consciousness is lost and the patient either dies or remains in a prolonged coma. Because of this, patients with DAI who have lost consciousness yet continue to live tend not to regain consciousness but remain in a prolonged coma. With increasing blood loss the patient may suddenly experience seizures, hemiparesis and eventually loss of consciousness. As the hematoma increases in size and compresses and damages the brain the patients symptoms become more severe and consciousness may again be lost. Because the skull is rigid and relatively inflexible, pressure is thus exerted on the soft tissue of the brain which in turn becomes compressed.
Nevertheless, force will be exerted from a high pressure region into a low pressure zone causing displacement of the brain.
This lead to respiratory and vasomotor abnormalities, and eventually loss of consciousness. The patient is disoriented, shows fear and irritability, over-reactivity and faulty perception of sensory stimuli sometimes accompanied by visual hallucinations. For example, those with a score between 3-5 have a mortality rate of approximately 60%, whereas individuals with a coma score of 6 or 7 who are between the ages of 30-50 have about a 50-50 chance of living or dying. In fact, these bumps may also damage the skull, burst blood vessels, and cause the brain to slosh around inside the cranium causing extensive cerebral injury. Moreover, although generalized recovery is often noted within 3 months of injury, a memory disturbances often remains and may in fact persist for years.
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. That is, if the post-synaptic neuron is injured, axonal transport to the damaged cell may become abnormal, such that in addition to a buildup of neurotoxicity, therby giving rise to neurofibrillary tangles, amyloid plaques, and cell death. Indeed, because these strains are not uniform but effect various parts of the cerebrum differently, such that one part of the brain is moving in one direction whereas another portion is sliding at a somewhat different angle, certain regions can literaly snap and break loose.
Interestingly, This condition occurs more frequently among individuals who do not suffer skull fractures.
If blood loss continues there is a great threat of temporal lobe herniation and eventual crushing of the midbrain. Sometimes the brain is displaced over or under the dura causing tearing and further compression effects. The Glasgow Coma Scale (GCS) in effect provides standardized criteria for the assessment and description of head injury severity. Disturbances in motor function are often indicative of widespread cortical or brainstem damage. This usually gives a family member or an inexperienced physician the erroneous impression that there is cognition. The frontal bone constitutes the skeletal framework for the forehead (including the orbits for the eyes) and is joined to the parietal bones (the bulging topsides of the skull) by the coronal sutures. Moreover, 3% of those with mild head injury will develop increased intracranial pressure and life-threatening hematomas which must be removed (Dacey et al.
If less severe there may be a temporary inability to function due to strains involving the axonal membrane (Adams et al. Hence, these disturbances are life-threatening and requires surgical intervention and identification of the bleeding vessel. Nevertheless, depending on where the brain is displaced, various types of herniation and subsequent brain damage may result. This form of herniation can also occur secondary to an expanding fronto-temporal lobe hematoma.
Usually the oculomotor nerve becomes compressed which causes ptosis, pupil dilation, and loss of eye movement. In contrast, a patient may seem to have sustained a mild skull injury and later demonstrate moderate to severe cognitive loss. Inappropriate verbalizations (yelling, swearing) are given a rating of "3", and incomprehensible verbalizations limited for example, to moaning, are scored "2". Moreover, sometimes the actual deficit is greater than the patient realizes (Prigatono et al.
Comprising the lower and lateral portion of the cranium including parts of its floor are the temporal bones which also house the structures of the inner ear. Indeed, about 50% of those who suffer mild head injuries are at risk for developing post concussion symptoms (PCS). The emotional disturbances may persist for months or years, but usually lessens as time passes. Contusions are often associated with this type of injury (Leestma 1991; Unterharnscheidt, & Sellier, 1966). Indeed, approximately 1 out 100 individuals with mild head injury die (Luerssen et al., 1988). In addition, the brains blood and oxygen supply can be reduced or diverted following chest injury, scalp laceration, or fractures involving the limbs.

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