Types and Degrees of Cranial Trauma

Head injuries can be roughly divided into two major groups that may overlap: (1) extracranial, where the coverings of the scalp, bone, membranes, or the brain are penetrated (immediate treatment is necessary to prevent infection leading to meningitis); and (2) intracranial, where the brain itself or its membranes are injured without the added complications of an external wound. In the latter event, the problem varies according to the extent of brain or membrane damage and to increased intracranial pressure.

Fortunately, instances of major head injury are rare as compared to the effects of accumulated minor trauma to the head. Minor impacts resulting in variable degrees of stuns, black-out, memory loss, and headache are often the responsibility of the team, company, or family doctor who must recognize the potential dangers and evaluate noxious signs and symptoms. While losses of consciousness or posttraumatic headache are common in contact sports and after falls or blows to the head, they do not represent diagnostic significance in themselves. But they do offer a starting point for observation and thorough investigation.

Mild head injuries do not usually give rise to unconsciousness, cranial nerve palsies, or focal contusion. If the injury is a little more severe, the patient feels momentarily dazed and may have a headache for some hours thereafter but, as a rule, suffers no other ill effects. Relatively trivial injuries can also produce disproportionately severe symptoms in patients who have had previous cranial trauma.

With severe injuries, consciousness is lost instantly. Respiration may cease, and all reflexes are lost. Within a few seconds, breath returns but unconsciousness continues. This stage may last minutes or days and may be followed by deepening coma and a rise in blood pressure or by a phase of cerebral irritability from blood in the cerebrospinal fluid. Seizures may occur. In the absence of massive intracranial bleeding, deepening coma usually means increasing intracranial swelling impairing cerebral circulation. A return of consciousness features irritability, confusion, disorientation, and a degree of amnesia.

Brain compression is always a danger in head injury. It is usually the result of hemorrhage into the middle or anterior fossa of the skull, but it may be the result of aerocele, increased cerebrospinal pressure, encysted collections of cerebrospinal fluid in the subdural or subarachnoid spaces, extradural hemorrhage, subdural hematoma, or edema from infection.

Emergency Treatment of Head Wounds.   Assure an open airway, and keep the patient's vital signs carefully monitored. Prevent or treat shock, but do not place the patient in the head- low position. Control bleeding, and protect the wound with a sterile dressing. Do not remove or disturb any foreign material that may be in the wound.

Closed Skull Wounds

Except for a possible bruise or contusion, there is no obvious external damage in closed wounds. Injury may be to the brain itself or to the pia or arachnoid meninges. Rupture of blood vessels in the pia is particularly important in closed injury. Blood spilled onto brain cells is a highly irritating foreign substance that disturbs the functioning of these tissues. Blood collecting under the skull exerts pressure against the brain. If there is no skull fracture or if skull fracture is such that the integrity of the dura is not disturbed, the cranium is unyielding. If the skull is depressed or displaced inwardly, it may exert direct pressure on brain tissues even without the formation of a hematoma. A fall on the back of the head will often cause more internal damage than a strong blow to the anterior head with a fist.

Clinical Signs.   Headache, nausea, dizziness, and loss of consciousness (which may be brief, intermittent, or extended) often accompany a closed head injury, depending on the particular injury and its severity. If injury is from impact with a blunt surface (common in sports), an elevated contusion forms when blood and other fluids collect in a pocket in the subcutaneous tissue between the skin and the skull. There may be a fracture in which part of the skull is displaced inwardly. In more severe injuries, vomiting and paralysis of some muscle groups occur. The patient may bleed from the nose, mouth, or ears in the absence of obvious injury to these parts. Cerebrospinal fluid dripping from the nose or ears indicates a grave injury. Normally clear cerebrospinal fluid becomes cloudy when mixed with small quantities of blood.

Signs of increasing intracranial pressure include elevated blood pressure, slow pulse, restlessness, dilation of one or both pupils, decreased respiration, cyanosis, delirium or irritability, and paralysis. Unless a surgeon is available soon to relieve pressure by opening the skull, increasing respiratory failure, heart failure, and death may be expected.

Open Skull Wounds

The patient may be either conscious or unconscious. Signs of intracranial pressure and internal damage, if any, are the same as for closed injury. Open wounds of the head are classed according to whether the integrity of the dura is disturbed. Two types are seen: those that perforate the dura mater and those that do not. Detail descriptions of these surgical emergencies are beyond the scope of this text.


Contusions and Lacerations

In definite injury to the surface of the brain, edema and ecchymosis with loss of function of the area involved result. Shock is commonly associated, unconsciousness and amnesia are more prolonged, and headache is more severe in the acute stage. Disorientation and mild confusion are usually exhibited and may exist for many hours or days following injury. General or focal convulsions occur, and paresis or paralysis of the cranial nerves or extremities are seen depending on the area of the brain involved.

Giddiness and transient postural unsteadiness may be seen. Intracranial pressure is usually increased, and the spinal fluid is blood tinged. Blood in spinal fluid interferes with its circulation and absorption, encouraging mechanical hydrocephalus, confusion, and increased headache. In severe cases, a permanent intellectual defect may persist, varying from minor memory failure to profound dementia.

Scalp Contusions.   Scalp contusions are either circumscribed or localized (producing a scalp hematoma) or sometimes accompanied by brain concussion. A depressed skull fracture may be falsely suspected because most of these blood pools are depressible in the center and offer the sensation of indentation of the skull.

Scalp Lacerations.   Lacerations of the scalp bleed profusely because the blood vessels, which are quite numerous, do not constrict. They retract as do vessels in other areas of the body. Scalp lacerations gape open because the intact scalp envelops the skull quite tightly. A severely fractured skull may be malshaped, yielding, or minus parts. In scalp lacerations associated with compound fractures, the prevention of sepsis leading to meningitis is the principle aim in emergency care. The subarachnoid space is protected by the skin, galea, and, in certain areas, by temporal and occipital muscles, pericranium, bone, dura, and arachnoid. The deeper the penetration of the wound, the greater chance of meningitis and thus the necessity of alert care in preventing infection.

Cerebral Contusions.   Cerebral contusion is a bruising of the brain difficult to distinguish from concussion unless it causes an increase in intracranial pressure. Contralateral localizing signs are usually seen opposite the bruise or hematoma. If the contusion or hematoma is on the same side of paralysis, there is possibility of contrecoup injury.

Cerebral Lacerations.   Cerebral laceration is a medical emergency that often follows severe trauma, particularly contrecoup injuries. Shock is invariably present, confusion and disorientation are severe, wild restlessness is pronounced, and deep stupor may prevail. General muscle flaccidity and loss of sphincter control are common. Marked neurologic changes feature abnormal reflexes, pupillary changes, paralysis, aphasia, and cranial nerve disorders. Other characteristics include respiratory irregularity, increased pulse pressure, slow pulse, fever, meningismus, possible convulsions, bloody spinal fluid, increased intracranial pressure, slow return to consciousness, prolonged headache, and amnesia.

In cerebral contusion or laceration, weakness or paralysis of the face or extremities appears immediately after injury and increases very little if at all. Thus, this time of findings and lack of progression are an important differentiation from an intra- or extra-dural hemorrhage.

Extradural Hemorrhage

The common clinical picture is a patient who has received a head injury and suffered a momentary loss of consciousness that is followed by complete or partial recovery. This lucid interval of recovery may last from a few hours to 2 days. Then, rather abruptly, a focal convulsion or rapidly progressing stupor, slow pulse and respiration, unilateral pupillary dilation, and weakness of face and extremities offer evidence of a localized expanding lesion. This important lucid interval is sometimes obliterated if the initial injury causes prolonged unconsciousness.

Typical features are early but brief unconsciousness followed by drowsiness, headache, vomiting, and hemiparesis. Immediate surgical intervention is required. Extradural hematoma is indicated by hematoma of the temporalis muscle, gradual onset of hemiplegia, deepening coma, Hutchinson's pupils, and a lucid interval. A signal of an extradural hematoma is the appearance of paralysis of the arm, leg, and face on the contralateral side of the lesion. The semiconscious patient will not respond to supraorbital pressure on the affected side.

When hemiplegia is suspected, corroborating signs must be sought such as increased deep reflexes, absent abdominal reflexes, and positive Babinski. In early cases, the arm is more affected than the leg. In cases of intracranial hemorrhage, Babinski's sign is most significant and the one most frequently present. It usually denotes a hematoma on the opposite side of the brain. Aphasia may be the first lateralizing sign in a left side lesion in a right-handed person. Broca's area is usually on the left side.

Extradural and subdural hematomas may be associated with either opened or closed head wounds and possible fractures. For example, a hematoma discovered in the temporal area suggests possible temporal fracture with meningeal artery laceration and associated epidural hematoma.


Acute Subdural Hemorrhage

This type of intracranial bleeding is much more common than extradural hematoma. It is usually associated with cerebral laceration and produced by a rupture of the veins spanning between the dura and arachnoid membranes. Although larger in size than an extradural hemorrhage, a subdural hemorrhage is confined unilaterally because the dura is firmly fixed to the falx between the hemispheres.

Acute subdural hematoma is the most frequent cause of death in sport injuries. The incidence is high in the elderly because cortical atrophy increases the space in which the veins must traverse. The incidence is also high in boxers, other contact- sport athletes, and alcoholics because of increased head trauma.

Subdural bleeding shows no lucid interval. Lateralizing signs are similar to those of extradural hemorrhage. Inequality of pupils (anisocoria) is an important localizing sign, and Hutchinson's pupil from compression of the 3rd cranial nerve against the free edge of the tentorium often occurs. Widely dilated and fixed pupils bilaterally indicate that death is near. Thus, on-scene frequent examinations of the pupils are necessary. Subdural hemorrhage is also characterized by headaches, drowsiness, poor concentration, mild confusion, progressively decreasing level of consciousness, and motor deficits (eg, hemiparesis). It is important for subsequent attending physicians to realize that these symptoms may be immediate or delayed for weeks or months after injury.


Chronic Subdural Hemorrhage

This pending emergency features symptoms of anorexia, vomiting, blurred vision, drowsiness, personality changes, and gait disturbances. These not infrequent sequelae of head injury are often related to a mild initial cranial trauma insufficient to cause loss of consciousness. The accident is often forgotten by the patient. Headache, mental changes, and drowsiness develop some months later.

Symptoms are often marked on one occasion, disappear, and return later with greater severity. Albuminuria is a striking concomitant finding, and xanthochromic spinal fluid is common. Motor involvement, emotional disturbances, and greatly altered deep reflexes are found. Less frequently, cranial nerve involvement, Jacksonian convulsions, aphasia, vomiting, slow pulse, and choked disc exhibit. The syndrome is produced by the clot attracting nonprotein fluids that cause gradual enlargement of the mass; ie, the osmotic tendency of any fluid of lighter density to pass through a semipermeable membrane to join fluid of greater density.


Depressed Fractures

Differentiation between hematoma and a depressed fracture is made by evaluating the edges of the lesion. The edges are usually smooth in hematoma and the circumference is rather regular. In depressed fractures, the edges are usually rough, irregular, and sloping. Careful pressure over a hematoma will ordinarily push aside any central indentation; but in fracture, no such shifting of the depression occurs. Roentgenography, however, offers the only reliable evidence.


Cranial Concussion

A pure concussion syndrome is rare. Most head injuries are accompanied by some degree of brain injury with a reaction similar to injury found in other tissues. The injurious forces usually result from acceleration, deceleration, or compression of the head or a combination of these factors.

Brain concussion is the most common injury to the brain following a cranial blow. It is defined as an essentially transient state due to head injury that has an instant onset, manifests widespread purely paralytic (flaccid) symptoms without neurologic evidence of gross brain injury, and is always followed by a degree of transient unconsciousness and amnesia for the actual moment of the accident. The degree of posttraumatic amnesia appears to be a guide as to the severity of the concussion. Unconsciousness may be prolonged, and reflex changes and even convulsions may manifest (especially in children). Edema and congestion occur that are coupled with a moderate rise in cerebral venous pressure.

The spinal fluid is always clear, and intracranial pressure is rarely elevated. Headache is often the sole post-traumatic complaint, but shallow breathing, pallor, feeble pulse, reduced reflexes, and other signs of surgical shock may result. Visual impairments, equilibrium disturbances, and memory failure are common. The period of short-duration unconsciousness after concussion is attributed to the momentary compression of brain capillaries resulting in cerebral ischemia/anemia. Any prolonged period of unconsciousness or inequality in pupil size indicates the need for neurologic consultation.

Hirata of the University of South Carolina wrote that by the time he arrives on the field at the side of an injured player (20-30 seconds) and the player is awake, able to think and answer questions, recognize others, and follow instructions, the player has not had a true concussion. A slight tap on the side of the face of a dazed player often results in arousal. If cranial nerve tests show normality, careful questioning receives rational answers, and responsibilities in play are alertly discussed, a return to action (under careful observation) can be made after a short rest.

If the player is disoriented 20-30 seconds after impact, however, he can be considered to have some degree of concussion. This requires restriction from play for 1-10 days wherein neurologic tests, vital signs, and subjective complaints are carefully monitored. Return to play can be made only after clinical signs are normal, the player is completely free of headache, and verbal-cognitive responses are normal. Skull films and cerebrospinal taps are not routinely ordered.

The typical athlete will shortly recover consciousness after a "knock out". There will be no retrograde headache, vomiting, or abnormal neurologic signs. Still, such a player should be accompanied home, be strongly advised to go to bed immediately, and seek follow-up examination the next day. Any player that must be carried from the field or ring deserves hospitalized observation and neurologic evaluation for at least a day or two. Poorly conditioned nonathletes require much more detailed examination and monitoring.


Skull Fracture Screening

Although x- ray proof of fracture is important, many fractures are difficult to demonstrate; clinical evidence may be more important. The examiner should carefully palpate the skull and look for small lacerations hidden within the hair. Skull fractures may be divided into two major groups: linear and depressed. There may be bleeding or leakage of spinal fluid from nose, mouth, or ears; difference in size of pupils; blackening of tissues under the eyes; changes in pulse and respiration that are not necessarily compatible with the blood picture; and paralysis or twitching of muscles. Head and/or neck injury should be suspected in any unconscious person.

Certain signs point to specific sites of fracture. For example, a fracture of the temporal area is often associated with deafness and facial nerve injury. Bleeding from the ear with a subcutaneous hemorrhage over and below the mastoid area (battle sign) appearing 24-48 hr after injury is highly suspicious of a temporo-occipital fracture at the base of the skull. Periorbital ecchymoses (raccoon sign) may indicate a basilar skull fracture. A tight ecchymosis of the eyelids indicates a fracture through the corresponding orbital plate. Rhinorrhea is proof of a fracture through the cribriform plate or into one of the paranasal sinuses in the anterior or middle fossa. Cerebrospinal fluid escaping from the ear signifies a fracture through the temporal bone at the base of the middle fossa.

Roentgenographic Findings.   Abnormally lucent (overlapping bony margins) or dense lines (two thicknesses of bone in a focal area) should be sought as both occur with skull fracture. Bright view-box illumination of the scalp margins helps to locate a site of injury and to detect soft-tissue swellings.

The skull is subject to linear fractures that appear on the film as thin black lines with ragged edges that may run in any direction. They must be differentiated from suture lines, diploic veins, and other blood-vessel grooves -all of having fairly definite courses, smooth margins, but are lighter in color. Vascular markings are normally shaped as gentle arcs; fracture lines appear as straight lines or sharply angled lines that are more lucent than vascular grooves. Fractures split the entire thickness of bone, while vascular grooves occupy only a part of the bone's thickness. Fracture lines may open sutures or follow blood vessel markings, but they can usually be traced beyond the course of these normal lines. A fracture extending through the distribution of the middle meningeal artery can produce epidural hemorrhage within a few hours.

Both dislocation or separation may also occur through suture lines. In adolescents and young adults, suture lines are still present and measure less than 3 mm. Potential arterial or venous bleeding or thrombosis of the dural sinuses may be found at the lamboidal and sagittal sutures. Infrequently, a meningeal cyst may protrude through a dural tear and herniate into a fracture, gradually eroding bony margins and inhibiting healing. Comminuted and stellate fractures are generally obvious. A depressed fracture offers an appearance of a white line because of the overlapping margins of the break. Fractures of either the outer or inner table appear as thin black lines or areas of slightly irregular density and structure of the bone. A tomogram may be necessary for detection. A basilar skull fracture is the most difficult skull fracture to detect, and most always requires a basal view. It is frequently overlooked.

Pneumocephalus and pineal displacement are important findings. A slight collection of air (pneumocephalus) progressing along the meningeal margins is a roentgenographic sign of skull fracture. The air pocket appears on the film as an area of markedly diminished density (usually frontal). The pineal gland, located in the central portion of the brain, is calcified in 60% of adults, and it may calcify as early as 6 years. Displacement of this gland, noted on either A-P or lateral views of the skull, may be the only indicator of a hematoma producing structural shifts within the cranium.

Aerocele

The prerequisite for the formation of a typical aerocele is a compound fracture with a ruptured dura. This is especially common with a fracture that involves the base of the skull or the sinuses, particularly the frontal sinus. The aerocele is produced by the increased air pressure within the nasal cavity when the patient sneezes or blows the nose. During these events, bacteria may be forced through the fracture into the cranial vault.

A combination of symptoms practically pathognomonic for this condition is a history of cranial trauma followed by sneezing which produces a sudden rhinorrhea. Coughing, sneezing, or nose blowing may force air within the cranium with the torn dura over the fracture line acting as a flap valve to prevent air from escaping. In roentgenography, air may be seen in the subdural space near the fracture, fill the subarachnoid spaces and reach ventricles, or be found within the substance of the brain itself. Symptoms suggest slowly increasing intracranial pressure.


Prognosis

There are four general signs helpful in determining outcome of brain injury: (1) the degree of initial subnormal temperature and shock, (2) the amount of blood in the cerebrospinal fluid, (3) the degree and length of stupor, and (4) the neurologic signs indicating the amount and location of cranial damage. The initial examination of an unconscious patient is always unsatisfactory. Pupil size and reaction, however, should always be noted. Fixed and dilated pupils present a poor prognosis. A unilaterally dilated pupil points to a unilateral brain lesion and sometimes is a more serious sign than bilaterally dilated pupils.

Tendon reflexes and clonus should be evaluated. Raising the extremities and letting them fall by gravity offers a fair opinion as to comparative limb power and tone. Complete muscular relaxation in all four extremities suggests widespread damage, as does a bilateral Babinski sign and ankle clonus. The eye grounds exhibit few clues in acute cases.


Controversial Consequences of Head Injury

Some authorities feel that trivial head injury may have serious sequelae while others insist on objective evidence of organic damage before acknowledging the likelihood of grave results. Some deny the possibility of permanent damage from a head injury with normal neurologic responses, normal spinal fluid, and normal ocular fundi or believe that a really serious injury is rare except in the presence of a fractured skull. Even the pathogenesis of the sequelae is controversial. Some authorities have found actual cerebral hemorrhage, often gross, as the substratum of the unconsciousness accompanying concussion. Others report hemorrhage in the areas supplied by the terminal vessels, and still others attach major importance to cerebral hydraulics, pointing out that the gnostic areas suffer more than the vital zones because the former are more recent in development, less important, and highly vascularized.

Prognosis is also controversial. Some authorities predict a gloomy outcome from minor injuries, stressing degenerative changes. Others reflect a more hopeful verdict, feeling that only in a small minority of instances do patients have lasting effects from head trauma. A claimant's attorney stresses the serious sequelae as it is impossible to make any infallible estimate of the nature and duration of the sequelae. Convulsions, photophobia, vertigo, weakness, and persistent headaches are sequelae common enough to merit consideration in any case. Insanity is a rare result (less that 0.01%), and the incidence of transient convulsions from severe head injury is about 4%-5%.


Syncope

Syncope is caused by three main reversible disturbances in cerebral function: (1) transient ischemia, (2) changes in composition of blood in the brain, and (3) changes in central nervous system activity by stimuli entering the central nervous system. When syncope results from arteriolar dilatation, it can be classified into three general types: (1) vasopressor syncope (common faint), (2) carotid sinus depressor reflex, or (3) postural hypotension from some disorder of the sympathetic nervous system.

Although fainting is often a fault of the cardiovascular system, neurogenic syncope is differentiated by a warning symptom (prodrome) that usually precedes the faintness. Coughing or some act eliciting orthostatic hypotension may be a precipitating factor. Hysterical syncope is differentiated by a lack of a history of injury, and the hysteric will always try to protect himself while falling if at all possible.


Vertigo

The causes of vertigo are head injury, viral labyrinthitis (aural vertigo), lesions of the 8th cranial nerve, lesions of the brain stem, temporal lobe, or cerebellum, disorders of the forebrain (eg, migraine, epilepsy), cerebrovascular disease, psychogenic dizziness (eg, anxiety and hyperventilation syndromes), ocular vertigo and motion sickness. Many drugs (eg, alcohol, barbiturates) give rise to dysequilibrium sensations. Infrequently, a metabolic process such as hypothyroidism may be involved.

Vertigo implies a hallucination of turning or rotating either of the self or the surroundings. The fault can be any place from the middle ear (semicircular canals, labyrinthitis) to the brain stem through the 8th cranial nerve. Pallor, sweating, and nausea are commonly associated. A related hearing loss or sensitivity to noise points to involvement of both divisions of the vestibulocochlear nerve. Dizziness in athletes is often caused simply by anxious overbreathing causing reduced blood carbon dioxide that inhibits nutrition of the balancing center. Two classes of vertigo have been defined:

Central vertigo has six major types:

(1) vascular (infarcts, postural hypotension plus vascular disease),
(2) tumors in cerebellopontine angle,
(3) seizures from temporal lobe lesion,
(4) multiple sclerosis,
(5) trauma (cranial, whiplash), and
(6) inflammatory (eg, meningitis).


Peripheral vertigo has five major types:

(1) vestibular apparatus lesion (Meniere's disease, benign positional vertigo),
(2) peripheral nerve lesion (acoustic neuroma, vestibular neuronitis, diabetic neuropathy),
(3) skull fracture and trauma, especially of the temporal bone,
(4) vascular (acoustic artery occlusion), and
(5) various eye disorders. A comprehensive history and examination will help determine the anatomic site of the lesion and the disease process involved. The significance of vertigo cannot be judged until the cause has been determined. It may represent a benign self-limiting condition, or it might represent a life- threatening condition.

Diver's Vertigo.   Two uncommon types of vertigo are commonly associated with divers. One is called "whiteout" when a diver cannot see the bottom and becomes disoriented. Closing the eyes during an attack or following air bubbles up helps in reorientation. The second type is that of alternobaric vertigo occurring during a diving ascent where eustachian tube blockage causes middle-ear pressure build-up.

Meniere's Disease.   The vertigo associated with Meniere's disease is almost always associated with a hearing loss, tinnitus, and a peripheral vascular disorder. Neuropathy (eg, diabetic), multiple sclerosis, tumors in the cerebellopontine angle, and temporal masses may be involved. In the elderly patient, vertigo is often associated with vascular insufficiency of the peripheral acoustic artery or secondary to vertebrobasilar disease.

The results of chiropractic in the treatment of the vertigo associated with Meniere's disease and Barre-Lieou syndrome are extraordinary. Lewit writes of the relationship of the cervical spine to Meniere's disease (Review in Czechoslovak Medicine, 1961, VII:2) after 120 cases of Meniere's disease and similar forms of vertigo were sent by leading ear departments of Prague for manipulative treatment.

Seizures can sometimes be linked to a history of head trauma when the trauma is recent. Convulsive seizures may be the first sign of something more serious than simple concussion. It is important to determine where the seizure began if possible as it is helpful in the localization of the various cerebral centers. Small subdural hematomas can easily be overlooked that result in a meningocerebral scar.

Seizures rarely occur when skull fracture does not injure the dura. Focal seizures result from anatomic lesions, while generalized seizures from the start are caused by metabolic or unknown lesions (presumed functional) such as grand mal and petit mal. Psychomotor seizures, often denoting temporal lobe disease, are characterized by episodes of behavioral changes and perception alterations.


Coma and Convulsions

Coma is a medical emergency, and at no time should its seriousness be minimized. Life-sustaining measures always have precedence over diagnostic procedures. Quick evaluation of the patient's respiratory and cardiovascular state is necessary. This includes assuring that the patient has an adequate airway and noting if he is hypotensive, in shock, or bleeding.

Proper emergency procedures must be instituted if any of these conditions exists. The causes of coma are almost identical with those of convulsions. Nearly every disorder that causes the one may cause the other. Either or both may result from cerebral concussion, brain compression, sunstroke, apoplexy, epilepsy, toxemia, diabetes, drugs, and Stokes-Adams syndrome.


Cerebrospinal Fluid Circulatory Disturbances

Impairment to normal cerebrospinal fluid circulation (CSF) results in a back-up in the ventricles leading to an increase in intracranial pressure. Severe facial or skull trauma, edema, meningitis, brain mass, or anything that will cause blockage along the passageways will produce fluid accumulation in the system resulting in a degree of hydrocephalus.

Signs of early increased intracranial pressure include yawning, hiccuping, and projectile vomiting. In a few days or weeks, high pressure inside the sleeve of the dura surrounding the optic nerve may cause the retinal veins to dilate and the pale pink optic nerve head to exhibit papilledema and a choked disc. A mass compressing part of the ventricular system is the most common cause of papilledema. It is commonly associated with headaches (dura mater stretching) and vomiting (parasympathetic reflex).


Infection

Meningitis.   Meningitis is the most dreaded complication of cranial trauma. It frequently follows a compound fracture with cerebrospinal leakage but sometimes accompanies poorly treated scalp lacerations that suppurate. Common features are headache, stiff neck, positive Kernig's sign, rapid temperature rise, and cloudy spinal fluid from bacteria and white cells.

Brain Abscess.   Brain abscess is a late and infrequent complication of head injury that usually results from a depressed fracture or penetration of a foreign body. Features include a period of mild chilliness and malaise followed by a normal or subnormal temperature as the abscess forms. Dulled mentality, slowly progressing signs of intracranial pressure, slight or severe headache, possible vomiting and choked disc, and neurologic evidence of an expanding lesion are also characteristic.

Cerebral Fungus.   In a compound fracture with considerable bone and dura loss, a cerebral fungus infection sometimes follows. This serious complication, often unavoidable, is characterized by spreading infection, edema, herniation, and abscess formation.

The Cranium

The dura matter of an adult does not adhere to the entire skull. Thus, it is possible for fluid to be forced between the cranium and the dura. The resulting increased pressure tends to dislodge attached dura from its points of skull connection. Branches of the middle meningeal artery nourish both the dura and the surrounding bone of the skull. If torn, bleeding forms between the skull and the dura to produce an extradural hematoma.

Craniospinal Dynamics.   Cranial trauma may effect motion of skull interfaces. While the cranial sutures are immovable in cadavers and anatomic specimens, they are slightly movable in the living body -despite teachings that they are not. The two uniting and five intervening layers between the edges of adjacent bones in the skull offer a strong bond of union but one permitting definite but limited movement.

This movement is necessary for tissue respiration of the brain and spinal cord. It is controlled by the following structures and motions: (1) the inherent motility of the brain and spinal cord, (2) the fluctuations of the cerebrospinal fluid, (3) the mobility of the intracranial and intraspinal membranes, (4) the articular mobility of the cranial bones, and (5) the involuntary mobility of the sacrum between the ilia.

Involuntary CNS Motion.   Every organ in the body exhibits a pulsation or inherent rhythmic action featuring a slow sinuous motion. The brain and spinal cord are no exception to this. They exhibit a slow rhythmic coiling and uncoiling of the hemispheres and a longitudinal movement of the spinal cord within the spinal dura. This combined motility of the CNS and movement of the cerebrospinal fluid effect a hydrodynamic "pump" and a bioelectric interchange. With very light cranial palpation, this pulsation can be felt to have a rate of about 10-14 cycles/minute. It is the result of the pull of the dural membranes, the fluctuating cerebrospinal fluid, and the inherent motility of the CNS. The sphenobasilar symphysis appears to be the key cranial articulation.

Before 25 years of age, it has a cartilaginous union; in later years, its resiliency is that of cancellous bone. Flexion of both the sphenoid and occiput increases the dorsal convexity and results in elevation of the sphenobasilar symphysis towards the vertex. Extension does the reverse. In other words, flexion of the midline bones appears as a slight increase in convexity; extension, a slight decrease in convexity. The paired bones move in synchronized internal and external rotation with those of the midline.

While cranial nerve involvement, weakness, or paralysis frequently follow severe head injury, the most frequent and annoying posttraumatic symptoms are frequent headache and transient vertigo. These purely subjective complaints are often difficult to judge. Basic differential aids are shown in Table 1.


Table 1.   Differentiation of Common Headaches

Symptom/Sign	Occipitocervical Neuralgia	Trigeminal Neuralgia	Vascular Migraine;	Temporo-Mandibular Traction
Pain	Throbbing, paroxysmal	Excruciating, paroxysmal	Severe, paroxysmal	Severe, dull
Quality	Muscle spasms	Stabbing	Throbbing	Dull ache
Location	Occipital	Facial	Unilateral	Facial
Aura	None	None	Visual	None
Duration	Days	Brief	Hours	Chronic
Associated symptoms and signs	Earache Eye pain Neck pain Paresthesias Anxiety Tinnitus Nausea	Trigger zones	Vomiting Photophobia Irritability	Bruxism Malocclusion Earache Joint clicks

Mechanisms

One or more of six major mechanisms is involved in headaches: traction, distention, inflammation, pressure, spasm, and referred pain or vasomotor dysfunction. There can be abnormal traction or compression on spinal and suboccipital nerves. There can be traction on veins and displacement of the venous sinuses producing headaches, or traction on or distention of the meningeal arteries and large arteries at the brain base. An inflammatory process or pressure mass involving any of the pain- sensitive brain structures will result in headache. Spasm of the cranial or cervical muscles will result in headaches quite frequently. Noxious reflexes arising in the lower back and as remote as the feet have been associated with headache.


Types

Chronic or Recurrent Headaches.   All complaints of frequent headaches require a detailed case history. The site of pain is important as a general rule of thumb holds that pain originating above the tentorium moves across the 5th cranial nerve and is perceived in the forehead, temples, and parietal areas of the skull. Pain that has its origin in the posterior fossa is carried across the 9th cranial and upper cervical nerves and is perceived in the occipital area.

Acute Headaches.   Recently acquired headaches may elicit associated symptoms of subdural hematoma, subarachnoid hemorrhage, systemic infection, seizures, and focal nerve deficits lending suspicion to meningismus, meningitis, brain abscess or tumor. Severe inflammations such as meningitis produce headache by direct involvement of the brain's pain-sensitive structures. The first concern is to see if the headaches are in any way associated with a life-threatening situation. Most life- threatening conditions have a short headache history of acute, severe pain with associated systemic symptoms. Virulent bacterial meningitis is characterized by acute illness, rapid advancing signs of meningeal irritation, and systemic infection. Symptoms are similar in viral meningitis, but the severity of symptoms is less. In granulomatous meningitis, signs of chronic organic disease stand out.

Tension Headaches, migraine, and cluster headaches are not usually considered to have a traumatic origin, but spinal injury, overstress, or a noxious viscerospinal reflex predisposing a subluxation complex may be in the history.

The Punch-Drunk Syndrome

Cumulative head trauma results in many boxers after fighting professionally or as sparring partners for 5 years or more. It is expressed as the "punch-drunk syndrome" and is sometimes referred to as dementia puglistica or progressive posttraumatic encephalopathy. Bowermann describes the early symptoms as mental confusion and slight unsteadiness of gait. Progressively, the individual may develop leg dragging, jerky responses, hesitant and slurred speech, hand tremors, head nodding, the expressionless facial features of Parkinsonism, vertigo, deafness, euphoria or aggressiveness, and finally, marked mental deterioration. More than half of all boxers with 5 years experience or more develop some degree of mental and emotional changes obvious to close associates. The syndrome may be either cerebellar or extrapyramidal oriented.

While the point of impact in boxing may be the chin, the greatest damage is probably produced by concussive forces transmitted to the area of the brain stem at the base of the skull. This is also true with blows to the side of the head that result in sharp lateral or rotational shearing near the atlanto- occipital joints. With a knock-out blow to the head, brain damage may result from the blow itself or just as easily and more seriously from the fall to the floor or canvas.

On autopsy of a victim, the hippocampus typically shows senile plaques, changes within its vessels, neuronal degeneration (Alzheimer's), decreased cortical neurons, subarachnoid adhesions, increased gliosis, an encysted hematoma, frontal lobe atrophy, many aged extradural and extra-arachnoid clots, fibrous thickening and localized scarring, defects in the deep layers of the septum pellucidum, and possible thrombosis of the superior longitudinal sinus and its parietal afferents. Headache and vomiting are early signs of chronic inflammation and thickening of any of the three brain coverings (pachymeningitis). Subdural hemorrhage, areas of diffuse small hemorrhages within the brain, cerebral edema, and/or thrombosis of superficial and deep vessels may result.

The findings described above are the opinion of most authorities. However, Kaplan, who for many years conducted pre- and post-fight electroencephalographs of boxers for the New York State Athletic Commission, believes that the "punch-drunk" syndrome is a myth. He states that more than 6,000 EEG records of boxers (many repeat recordings over several years) show no changes of altered brain electrical activity to suggest any degree of diffuse petechial brain hemorrhage. Other EEG studies of boxers show that interval alpha-rhythm increases do not persist after 4 minutes following a fight. However, if persistent focal changes do occur on EEG graphs (eg, incipient epilepsy signs), boxing should be permanently banned for the athlete.


Craniosacral Therapy

Osteopathic colleges have done considerable research in this area. It is not a new concept within chiropractic, but one frequently overlooked. Willard Carver discussed cranial adjusting in cases of hydrocephalus as early as 1906, and later Drain and Spears wrote of its effectiveness in various types of cases. Distortion as far away as the feet have been showed to have a distinct effect on the sutures of the skull.

As cranial distortion always follows the lines of least resistance in conformity with the anatomy of suture closure, adjustive procedures must take this into consideration. Patients are usually adjusted in the supine or lateral recumbent position depending on the suture involved. The head should be supported with a firm pillow. A broad palm contact supported by a stabilizing hand is used. The mechanism of adjustment is more of a gentle pumping traction than a thrust.

It's recognized in chiropractic that sacral imbalances will affect higher spinal segments, and vice versa. Fairly new to these biomechanical manifestations within the kinematic chain, however, is the recognition of the influence on the cranium and TMJ and their part in contributing to the overall adverse neuromusculoskeletal synergism involved. Berkman found that the jaw influences the holding power of the atlas and axis, and, in turn, subluxations of the atlas and axis affect the stability of the TMJ. The fascia colli bind the jaw and cervical spine into a unit where a fault of any one part will influence the entire mechanism.

Involuntary Sacral Motion.   Besides normal voluntary and postural motions of the sacrum between the ilia and L5, the sacrum responds to the inherent motility of the CNS, fluctuation of cerebrospinal fluid, and pull of the intracranial and intraspinal membranes in a similar fashion as do the cranial bones. With light palpation, it is felt as a slight rocking synchronized with cranial motion. Dysfunction of inherent craniospinal motion is also noted in every case of TMJ pain and dysfunction, thus the wide range of effects -from cranial nerve involvement to lower extremity disorders. Likewise, the spine, pelvis, and extremities also affect the head and TMJ via the temporals because there is a direct dura attachment of the sacrum to the cervical spine and occiput.

The incidence of facial wounds has been greatly reduced in athletics through the mandatory use of protective equipment in some sports, yet injuries commonly arise when protection is not provided.

Background.   Bleeding from wounds of the face is usually profuse because of the many regional blood vessels. Hemorrhage is difficult to control. The upper airway may become obstructed by blood, mucus, or foreign matter causing respiratory failure and death. Maintenance of an open airway and control of hemorrhage are the emergency procedures taking priority.

First Aid in Face Wounds.   Clear the airway if necessary. Check for signs of head injury. More than any other area of the body, injuries to the face and jaw are likely to produce upper airway obstruction. In jaw fracture, the tongue may fall backward or blood may gather in the hypopharynx. The patient is placed in the semiprone position to allow drainage of the airway. Prevent or treat for shock, which is always a danger. Prevent chilling or overheating. If the patient prefers, he may sit on the ground with knees drawn up and with his head resting on his arms folded across his knees.

Except for minor wounds, surgical consultation should be sought immediately. Digital pressure can be applied to appropriate pressure points to control hemorrhage. In minor abrasions of the face or skull, bleeding can be stopped with cold and compression, and the wound can be washed with a tepid saline solution. In more serious cases, a layer of foam under the pressure pad may be necessary. Many recommend dusting the wound with an antibacterial powder. A sterile pressure dressing and cold pack should be applied over skin wounds, but never place a dressing within the mouth.

Nasal Trauma

In the typical broken nose, the bridge of the nose will be bruised and show a definite depression (if not obliterated by swelling). When viewed from the front, the nose will deviate from the midline. Hematoma and/or infection are always a threat.

Epistaxis.   Facial contusions and nosebleeds are common in sports and exhibit an excellent need for ice, compression, and elevation (I-C-E). Nose injuries are invariably accompanied by profuse bleeding. Ice or another source of cold should be applied with the nostrils compressed. The part is elevated by having the patient sit with his neck hyperextended. In severe cases, the nose is packed with ribbon gauze and the patient is referred for cauterization or to surgical attention.

In cases other than direct trauma, cracking of dry nasal mucous membranes, coagulopathy, hypertension, Weber-Rendu-Osler syndrome, or barotrauma may be a factor. The latter situation is seen in scuba divers where poor pressure equalization within sinuses causes facial pain followed by unfrothy sinus bleeding into the nose and/or mouth.

Fractures.   These are rarely viewed in roentgenography during the early stages because severe damage is usually restricted to cartilage. Nasal fracture with displacement requires quick reduction. Later, positive x-ray findings are the result of healing by fibrous union between fragments. Examination must be made immediately before swelling takes place or wait until swelling subsides. Deformity is difficult if not impossible to correct after 2 weeks from the time of injury without refracturing. Rarely, an acute hematoma develops between the cartilage and perichondrium, requiring cold, pressure by a nose pack, and aspiration. Infection offers the danger of cavernous sinus thrombosis and its life-threatening potential.

Dental Injuries

Contact sports have a high injury incidence to the teeth when protection is not mandatory. Over 20% of fractured molars have been traced to sports injuries, and front teeth are even more vulnerable. Tooth pain may or may not have a history of trauma. Pain on biting indicates decayed dentine, pain on eating sweets is usually due to decay, and pain on temperature changes points to pulpitis (eg, abscess). Gum tenderness dorsal to the molars suggests pericoronitis from an impacted wisdom tooth. A painful dental disorder may be brought out and isolated by lightly tapping the suspected tooth with a mirror handle. A blue-gray tooth is likely dead from an old infection. In any case, dental referral should be made for evaluation and treatment.

Tooth concussion usually results in little loosening or displacement, but sensitivity to biting pressure or temperature extremes may last for a time. However, a comparatively mild force against the upper front teeth can lead to fracture and dislocation. A displaced tooth always involves socket fracture. Tooth injury may vary from (1) cracked enamel of one or more teeth resulting in slight loosening (subluxation) and sensitivity to cold, (2) crown fracture involving tooth pulp, or (3) injury of one or more tooth roots. Severe pain usually indicates that fracture has exposed the pulp. During severe trauma to the teeth, the force may extend to the periodontal tissues.

Trigger points within the temporalis muscle frequently refer pain similar to facial neuralgia. Points within the anterior aspect tend to refer pain to the front teeth; the middle aspect, the incisor area; the posterior aspect, the molars and TMJ area.

Emergency Aid.   Temporary support can be given to a loose tooth with soft paraffin or candle wax heated to the form of masticated chewing gum. The patient should be instructed not to apply finger pressure to test the looseness of a damaged tooth. If complete avulsion occurs, the tooth should be wrapped in gauze and the patient and tooth immediately referred to a dentist for possible reimplantation. The dentist will wash and prepare it. Replacement in the socket must be done as soon as possible to be successful. The faster implantation and splinting are made, the better the results; and the younger the patient, the better the results. A replanted tooth is not permanent, but it may last 10-15 years.