Why don't helmets prevent the worst kinds of injury?

W. J. Curnow, The efficacy of bicycle helmets against brain injury, Accident Analysis & Prevention, Volume 35, Issue 2, March 2003, Pages 287-292.

Abstract
An examination is made of a meta-analysis by Attewell, Glase and McFadden which concludes that bicycle helmets prevent serious injury, to the brain in particular, and that there is mounting scientific evidence of this. The Australian Transport Safety Bureau (ATSB) initiated and directed the meta-analysis of 16 observational studies dated 1987-1998. This examination concentrates on injury to the brain and shows that the meta-analysis and its included studies take no account of scientific knowledge of its mechanisms.

Consequently, the choice of studies for the meta-analysis and the collection, treatment and interpretation of their data lack the guidance needed to distinguish injuries caused through fracture of the skull and by angular acceleration. It is shown that the design of helmets reflects a discredited theory of brain injury. The conclusions are that the meta-analysis does not provide scientific evidence that such helmets reduce serious injury to the brain, and the Australian policy of compulsory wearing lacks a basis of verified efficacy against brain injury.

Highlights:
The testing and design of standard helmets continue to reflect the discredited theory that linear acceleration is the dominant cause of brain injury and to neglect rotation. Ommaya et al. (1971) therefore called for revision of the standards, to include protection against its injurious effects, but to no avail.

2.3. Angular (rotational) acceleration
Holbourn (1943) proposed a theory of brain injury that has no role for linear acceleration as a direct cause and rejects the mechanism of coup/contre-coup. He started from the physical properties of the brain of being about as dense and incompressible as water and having low rigidity. Using models of the brain and skull, he deduced that linear acceleration arising from a blow produces only small shear strains which have no injurious effect on the brain. Forces of rotation, by contrast, produce large shear strains and cause the brain to slide along the internal surface of the skull. Blood vessels may then be ruptured, causing SDH. He attributed so-called contre-coup injuries to rotation.

Experimental evidence in support of Holbourn has since accumulated (Adams et al., 1982). Pudenz and Shelden (1946) observed, using high speed cinematography on monkeys with part of their cranium replaced with transparent material, that the brain rotated within the skull during impact and did not draw away from it.

From the 1960s, the heads of primates were subjected to controlled acceleration, both linear and angular. Ommaya et al. (1971) reported that such experimental work supported Holbourn's view that only skull damage and rotation of the head are important and that pure (linear) head translation had never been demonstrated as an injury producing factor for the brain. They dismissed a variation of the linear acceleration theory by Gross (1958), which proposed that a blow to the head generates pressure waves, causing cavities to form at the opposite side of the brain and injure it as they suddenly collapse. Ommaya and Gennarelli (1974) used apparatus that produced either pure translation or rotation of monkeys' heads through 45° without any impact and its possible confounding effects. They found that rotation resulted in paralytic coma or traumatic unconsciousness, but translation did not.

2.4. Diffuse injury
According to Henderson (1995), three out of four cases of brain injury sustained by road accident victims fall into the diffuse type, the commonest and mildest form being concussion. The severe form, now designated diffuse axonal injury (DAI), was first defined by Strich and Strich). Her microscopic examination of brain tissue of patients who suffered extreme dementia until death found few lesions visible to the naked eye, but widespread diffuse degeneration of the white matter. She attributed it to shear strains resulting from angular acceleration.

Graham et al. (1995) noted that DAI is the commonest cause of disability after head injury, including the vegetative state, and that it occurs mainly in road traffic accidents. In Glasgow, 45 out of 177 patients with fatal non-missile head injury were found to have DAI, judged to be identical to that produced in the subhuman primate by angular acceleration ( Adams et al., 1982). In Australia, 29 out of 62 patients fatally injured in traffic accidents had DAI of similar character ( Blumbergs et al., 1989) and the brain of a child pedestrian who died after being struck by a car showed injuries associated with angular acceleration ( McCaul et al., 1988).

The duration of angular acceleration is also a factor, as experiments with primates have shown. Over a short time at a high rate it mainly affects blood vessels, leading to SDH and contusions. A lower rate and longer duration produce DAI and traumatic coma (Adams et al., 1986).