Quoted message said:| > On another tack: does anyone know what deceleration rate causes brain damage (I have a
| > gruesome image of Eichmann finding this out) and how it relates to the maximum impact speed
| > for cycle helmets?
Quoted message said:This isn't about decelerating the head though. My thought was to find a comparison between the
minimum deceleration where you'll get brain damage versus the maximum deceleration a bike helmet
is intended for. If the latter is more than the former then bike helmets can't save anyone from
brain damage i.e. the shell cracks and the polystyrene doesn't significantly reduce the
deceleration.
You're making the same mistake helmet manufacturers and everyone else did. It's not necessarily the
deceleration that is doing the damage.
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).
