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Biomechanical Aspects

Each of the four different sources of bleeding has its particular underlying mechanism. The different types of SDH are summarized according to their pathogenetic features:

1. Recurrent "spontaneous" SDH undoubtedly exists (Matsuyama et al. 1997), although its pathogenesis has been questioned (Maxeiner 1997). Most spontaneous SDH are arterial in origin caused by a hypertensive peak in blood pressure or preexisting damage to an arterial wall (e.g., arteriosclerosis). A compromised vessel can also tear spontaneously. Spontaneous SDH is also associated with hematological or hepatic coagulation disorders and with anticoagulation therapy. A (secondary) SDH may result from the rupture of a cerebral arterial aneurysm or an intracere-bral angioma into the subdural space. Friede's (1971) electron microscopic studies of the dura showed that a subdural neomembrane may form even in the absence of a traumatic event due to a proliferation of dural endothelial cells; a secondary spontaneous SDH is possible in such cases

Scalp

Scalp

Brain Proliferation Peak
Fig. 7.12. Acceleration mechanism of the head which causes a tearing and stretching of the (blue colored) parasagittal bridging veins connecting the arachnoid and the dura (source: Wilson 1946; see also Sellier and Unterharnscheidt 1963)

(Friede and Schachenmayr 1978; Schachenmayr and Friede 1978).

2. Contusion-induced SDH arises when intracere-bral pressure causes tearing of, e.g., small cortical veins. The cavitation theory (see Chap. 9, pp. 179 ff) does not adequately account for such arterial tearing. Additional distortion of the vessels - such as that caused by an acceleration event - is required for tearing to occur.

3. Cortical lacerations associated with fissures, linear fractures or depressed fractures of the skull can cause SDH when arteries or veins are torn by sharp bone edges. Attendant lesions of the arachnoid will result in bleeding into the subdural space. In most cases, laceration or contusion injuries of the scalp are found at the site of impact.

4. Acceleration/rotational mechanisms (Fig. 7.12): SDH is less likely to be near the impact site than a contusion injury (even in the presence of a fracture). Thus, inertia is probably responsible for some instances of SDH (Ommaya and Gennarelli 1974; Gentleman et al. 1992). Gurdjian (1975) created experimental loading conditions that initiated rapid acceleration without impact to the head to show that acute SDH can be induced without contact. Biomechanical conditions sufficient to cause SDH can also be generated by a blow (assault) or fall. About 30% of all cases of SDH involve isolated SDH without associated skull fracture or cortical hemorrhages (Unterharnscheidt 1993; Graham and Gennarelli 1997; Maxeiner 1998), generally caused by acceleration (Gennarelli and Thibault 1982) or a blow.

Fig. 7.13a-d. Rupture of bridging veins along the sagittal fissure. nal lamina of the dura on the left hemisphere; d the vessel's rup-

a, b Seen at autopsy on the surface of the left brain hemisphere ture (arrows) on the crest of the first frontal gyrus of the right and and - a second case - c after formalin fixation demonstrating the left hemisphere is demonstrated on the frontal section bridging veins (arrows) connecting the arachnoid and the inter-

Fig. 7.13a-d. Rupture of bridging veins along the sagittal fissure. nal lamina of the dura on the left hemisphere; d the vessel's rup-

a, b Seen at autopsy on the surface of the left brain hemisphere ture (arrows) on the crest of the first frontal gyrus of the right and and - a second case - c after formalin fixation demonstrating the left hemisphere is demonstrated on the frontal section bridging veins (arrows) connecting the arachnoid and the inter-

Non-contact mechanisms usually produce no injury of the scalp. A blow to the chin, however, can induce rotational movement sufficient to cause tears of the bridging veins and/or cortical and basal arteries (Krauland 1982; Unterharnscheidt 1993). The resulting SDH may be bilateral or occur on the same or contralateral side of the impact. SDH may be induced in infants by shaking with or without accompanying impact (see Chap. 25, pp. 493 ff). In the elderly, SDH may occur without apparent or negligible head injuries.

Most SDH are located over the cerebral convexities, associated with cortical hemorrhages, and result from associated (indirect) tearing and stretching of the parasagittal bridging veins (Krauland 1961; Ja-mieson and Yelland 1972) that drain the surface of the cerebral hemispheres and the CSF into the dural venous sinuses. Parasagittal bridging veins are highly vulnerable to rupture from brief, high-velocity angular acceleration of the head (Gurdjian 1975).

If angular acceleration is low and of long duration, as often happens in traffic accidents, strains are propagated deep within the brain and cause diffuse axonal injury (DAI). Increased acceleration can result in acute SDH combined with DAI and torn-tissue hemorrhages (Gurdjian 1975). Such acceleration can be produced by falls in which the head strikes a hard surface or a blow, with broad impact and induced rotation. Seventy-two percent of acute SDH on file at the University of Pennsylvania Head Injury Center Data Bank had been attributed to a fall or blow, only 24% to motor vehicle accidents (Gurdjian 1975; Maxeiner 1998).

Rotation is most likely to cause tearing of the bridging veins along a transverse or diagonal-frontal axis, the greatest displacement of the skull relative to the brain occurring along the midline (Krauland 1982). If there is rotation around a transversal axis, which is often associated with translational acceleration, the brain is rotationally displaced against the skull in the parietal region, injuring the cortical arteries and inducing parietal cortical hemorrhages.

The macroscopic picture is dominated by the in-tracranial shift of brain tissue and edema, usually becoming apparent in the contralateral hemisphere through obliteration of the gyral sulci and flattening of the gyral crests. SDH is often attended by extensive subarachnoid hemorrhage (SAH). A circumscribed SAH may indicate the site of the torn bridging veins (Fig. 7.13).

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