cerebelli and change their extension whilst changing the patient’s position.

Subarachnoidal and intraventricular pneumatoceles impose on X-rays as a pneumo-encephalogram.

Pneumatoceles are a permanent risk of infection and will lead to rising intracranial pressure, especially if there is a unidirectional valve mechanism (Kretschmer 1978).

According to Probst and Tomaschett (1990), a major pneumocranium occurs in 22% of the cases with skull base fractures. In our own patient group with craniofacial fractures, 27% of the patients developed a pneumocranium (Figs. 6.3 and 6.4).

•It is often not possible to detect liquor leakages in the acute phase of craniofacial injuries. The radiological evidence of a pneumatocephalus is regarded as evidence of a possible dural injury

6.1.1.3  Meningitis

If therapy and trauma management are inadequate in open skull base traumas, the direct communication of contaminated, bacteria-loaded tissues or spaces within the intracranial space results in a potentially lethal infection risk (Entzian 1981; Dagi and Poletti 1983; Süss and Corradini 1984; Wilson et al. 1988; Wolfe and Johnson 1988; Hell et al. 1996).

The start of meningitis from within a few hours up until the first days following the accident is known as early meningitis. To ensure the diagnosis, a liquor puncture should be performed (Potthoff 1985).

The potential risk of developing meningitis in frontal skull base fractures varies from 25% (Jamieson and Yelland 1973; Flanagan et al. 1980; Dagi et al. 1983; Hubbard et al. 1985; Schmidek and Sweet 1988) to over 30% (Eljamel and Foy 1990), with a cumulative long-term risk of 85% within 10 years after the trauma. Surgical wound repair lowers the average risk from 30 to 4% and the cumulative risk from 85 to 7% (Eljamel and Foy 1990).

•The potential risk of a cerebral infection (meningitis, intracerebral abscess) lies between 25 and 30% in nontreated, traumatic frontal skull base defects (Loew et al. 1984; O Brian and Reade 1984).

The average risk of meningitis in a fracture of the posterior wall of the frontal sinus is calculated at 2.6–9%

(Hager 1986; Wallis and Donald 1988; Wilson et al. 1988; Miyazaki et al. 1991(1–3%); Schroeder 1993; Godbersen and Kügelgen 1998).

6.1.2   Uncertain Signs of Skull Base

and Dural Injuries

6.1.2.1  Lesions of the Cranial Nerves

Various trauma mechanisms can lead to specific cranial nerve lesions. If such lesions are detected, there is a high probability of a skull base injury (Potthoff 1985).

In midface/skull base fractures, neurological complications of extracranial origin occur in about 50% of the cases (Bonkowsky et al. 1989). According to Lee (1983), consequences involving neurological ocular motility occur in 17% as lesions of the cranial nerves III–IV–VI (30% cranial nerve III/14.5% cranial nerve IV/34% cranial nerve VI and 21.5% combinations of these nerves).

Olfactory Nerves

Frontal skull traumas are the cause of most unior bilateral injuries to the olfactory nerves (I) (unilateral or bilateral anosmia)

Possible causes are:

•a direct injury to the olfactory fibers

•a disruption of the fibers in a fracture of the cribriform plate

•a trauma-associated temporary injury of the olfactory bulb or tract

•a destruction or irreparable contusion of the olfactory bulb

•a cortical contusion and a contre-coupe damage at the bottom of the frontal lobe of the brain.

Indirect injuries of the olfactory filaments occur by overextension of the fine filaments induced by contusional dislocation of the brain, bleeding in the area of the olfactory bulb or by a hematoma in the perineurium of the olfactory ligaments. Contre-coup frontal lobe contusions may also cause an alteration in olfactory function. Posttraumatic dysosmia occurs in 5–9% of the cases (Lewin 1966).

In 50% of the traumatic dysosmia cases there is a complete bilateral anosmia, in 20% a unilateral anosmia and in the other cases a unilateral or bilateral hyposmia. A hyposmia usually has a good prognosis; whereas in an anosmia, the prognosis is bad (Kretschmer 1978).

There are different possibilities to test the olfactory sense: subjective olfactory sense test/simulation tests/ semiquantative determination of the olfactory sense/ objective olfactometry.

Oculomotor Nerve

The oculomotor nerve (III) is mostly damaged within the orbit or in the area of the superior orbital fissure. Ptosis, widened unresponsive pupils and immobility of the globe are characteristic for a complete loss of function of the oculomotor nerve. Partial paralysis is mostly limited to a ptosis, a restriction of cranial eye motility and abnormal pupil reaction.

Three outcomes are possible: (1) no recovery, (2) regenerative recovery and (3) aberrant regeneration.

Recovery may take between 6 and 9 months. When aberrant regeneration occurs, paradoxical eye movements are observed. Typically, eyelid elevation occurs on attempted adduction or downward gaze. Pupil constriction and accommodation may accompany downward­ gaze, with pupil dilation on abduction (Dutton and Al-Qurainy 1991) (Fig. 6.5).

Trochlear Nerve

Isolated paralysis of the trochlear nerve (IV) seldomly occurs in skull base fractures. This is mostly combined with defects in function of the oculomotor nerve. Reasons for damage are: skull base fractures in the region of the petrous bone, fractures of the greater wing of the sphenoid and of the temporal bone along the petrosquamosal fissure. Also intracranial injuries located at the top of the pyramids of the petrous bone can damage the nerve (Kessel et al. 1971; Kretschmer 1978). Frontal antero-posterior trauma is the most common cause.

The superior oblique muscle, which is innervated by the trochlear nerve, is responsible for depression of the globe in adduction and also produces intorsion. Vertical diplopia, which may be accompanied by torsional double vision, occurs in case of damage to the trochlear nerve. Spontaneous recovery may occur 3–6 months after injury (Dutton and Al-Qurainy 1991).

Abducent Nerve

The abducent nerve (VI) has a long intracranial course and is frequently damaged by direct trauma. Paralysis mostly occurs after skull base fractures, especially in fractures in the area of the petrous bone

— or as a consequence of raised intracranial pressure (ICP). Examination reveals a paralyzed lateral rectus

muscle and failure of ipsilateral abduction. Abducent nerve palsy may also result from a traumatic caroticocavernous sinus fistula.

Optic Nerve

The optic nerve is damaged in 2% of all closed traumatic cranial injuries (Holt and Holt 1983; Gossman et al. 1992) and in 20% of all frontal skull base injuries (Ioannides et al. 1988). The highest risk of damage exists in frontal (72%) and fronto-temporal (12%) traumas (Kline et al. 1984; Sofferman 1988, 1991).

Direct lesions of the optic nerve can be observed in skull base trauma caused by compression of the nerve during its intracanalicular course and/or by dislocated bone fragments compressing the nerve (Hardt and Steinhaeuser 1979; Lädrach et al. 1999).

Indirect lesions result from contusion, necrosis, rupture of the vessels, intracanalicular or/and intraconal hematomas. Also, secondary edemas and circulatory problems put the nerve function at risk. Indirect lesions are seen in 6.1% of the skull base fractures (Obenchain et al. 1973; Mathog 1992) (Fig. 6.6).

Fig. 6.6  Mechanism of injury to the optic nerve (schematic drawing). Indirect forces to the sphenoid bone lead to fragmentation of the sphenoid wing with intrusion/compression of fragments into the optic nerve (mod. a. Hardt and Steinhaeuser 1979, Lädrach et al. 1999). 1 Ophthalmic artery, 2 optic nerve, 3 bone fragment (sphenoid)

• A progressive loss of vision without injury to the globe or the bony orbital cone is most likely caused by an orbital hematoma and/or compression of the optic nerve in its intracanalicular pathway due to bleeding or edema (Lipkin et al. 1987; Stoll 1993; Rochels and Rudert 1995).

Loss of Vision in Midface Fractures

A loss of vision in midface fractures occurs in 15-20% of all severe midface injuries (Jabaley 1975; Holt and Holt 1983; Al-Qurainy IA et al. 1991 a, b, c; Dutton and Al-Qurainy 1991; Brown et al. 1999; Poon et al. 1999; Cook 2002; Manolidis et al. 2002; Soparkar 2005).

Injury to the optic nerve most frequently occurs in central fronto-naso-ethmoidal fractures due to fractures along the lesser wing of the sphenoid and seldomly in complex lateral midface fractures with fractures of the greater wing of the sphenoid (Ketchum et al. 1976; Kretschmer 1978; Hardt and Steinhaeuser 1979; Chilla 1981; Bleeker and Los 1982; Lipkin et al. 1987; Fonseca and Walker 1991; Vitte et al. 1993; Lädrach et al. 1999; Soparkar 2005; Stewart 2005).

Nearly 76% of isolated fractures of the sphenoid bone are associated with lesions of the orbit. There is a deterioration of vision in about 29% due to direct or indirect injury to the optical nerve (Hasso et al. 1979; Ghobrial et al. 1986) (Figs. 6.7 and 6.8).

Location of Optic Nerve Lesions

The most susceptible region for injuries of the optic nerve is located in the intracanalicular pathway from the orbital cone to the optic chiasm (Ramsay 1979; Gellrich et al. 1997). In 56% of the cases this is the location of trauma (Kessel et al. 1971). There are almost always associated skull base fractures, yet in approximately only 10% of the cases the fracture lines run through the optic canal or through the anterior clinoid process (Ramsay 1979; Leider and Mathog 1995).

The second largest group of injuries comprises injuries located in the area between the optical papilla and the point where the central retinal artery enters the optic nerve. These make up 13% of the injuries.

Injuries resulting from nerve tearing at the junction point with the globe ball form the third largest group with approximately 11.6% (Kessel et al. 1971).

Clinical Appearance

Visual reduction may vary from reversible to irreversible loss of vision with the preservation of globe motility (Lipkin et al. 1987; Gellrich et al.1996; Gellrich 1999). Clinically, either a bitemporal hemianopsia or an amaurosis (canalis opticus syndrome) with an intact concurrent reaction to light may develop in the involved eye.

In 34% of complex midface injuries with dysopia there is a reduction of vision, in 47–52% there is an immediate amaurotic damage and in 12–14% a protracted development of an amaurosis (Neubauer 1987) (Fig. 6.9).

CT Analysis of Optic Nerve Lesions (Gellrich 1999)

Primary CT Signs

•Fracture running through the optic canal, possibly with dislocated fragments

•Fracture in the retrobulbar orbital region, intraorbital bony fragments

•Soft tissue: optic nerve hematoma/edema, optic nerve swelling, interruption of the optic nerve, hemophthalmia

•Retrobulbar hematoma in the posterior third of the orbit