Endocranial Lesions in Non-Adults

International Journal of Osteoarchaeology
Int. J. Osteoarchaeol. 14: 8297 (2004)

Published online 10 March 2004 in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1002/oa.713
Endocranial Lesions in Non-adult

Skeletons: Understanding their Aetiology
M. E. LEWIS*
School of Conservation Sciences, University of Bournemouth, Poole, Dorset, UK
ABSTRACT
Reactive new bone on the endocranial surface of the skull in non-adults has recently received
a lot of attention in the palaeopathological literature. These features appear as layers of new
bone on the original cortical surface, expanding around meningeal vessels, as isolated
plaques, hair-on-end extensions of the diploe or, as capillary impressions extending into
the inner lamina of the cranium. These lesions are commonly found on the occipital bone,
outlining the cruciate eminence, but have also been recorded on the parietal and frontal
bones, and appear to follow the areas of venous drainage. Although recognized as resulting
from haemorrhage or inflammation, their precise aetiology is still a matter of controversy.
This paper outlines their possible causes and examines their nature and distribution in a
group of non-adults from four archaeological sites in England. It is recommended that, when
recording these lesions in the future, additional skeletal pathologies, the age of the child,
and nature and distribution of the lesions also be taken into account. Copyright 2004
John Wiley & Sons, Ltd.
Key words: endocranial lesions; aetiology; meningitis; differential diagnosis; growth
Introduction
Reactive new bone, located on the endocranial
surface in non-adults is a relatively new area of
investigation for childhood disease in the past.
These features either appear as diffuse or isolated
layers of new bone on the original cortical surface, expanding around meningeal vessels, as
hair-on-end extensions of the diploe, or as
capillary impressions extending into the inner
lamina of the cranium. The lesions are found on
the occipital bone, outlining the cruciate eminence, but have also been recorded on the
parietal and frontal bones and appear to follow
the areas of venous drainage. Various aetiologies
have been suggested for these lesions in the
literature including; chronic meningitis, trauma,
* Correspondence to: School of Conservation Sciences, University
of Bournemouth, Dorset House, Talbot Campus, Poole, Dorset
BH12 5BB, UK.
e-mail: mlewis@bournemouth.ac.uk
Copyright # 2004 John Wiley & Sons, Ltd.
anaemia, neoplasia, scurvy, rickets, venous drainage disorders and tuberculosis (TB). All may
cause inflammation and/or haemorrhage of the
meningeal vessels (Griffith, 1919; Kreutz et al.,
1995; Schultz, 1993a, 2001). Koganei first
described these lesions in 1912 and referred to
them as cribra cranii. He identified web-like
deposits on the internal surfaces of the frontal,
parietal and occipital bones during autopsy,
which sometimes communicated with the diploe,
as well as pitted and grooved lesions. However,
Koganei found endocranial lesions to occur more
often in adults than children, and more commonly on the frontal than any other part of the
skull. In 1961, Henschen also noted endocranial
lesions in a collection of Swedish skulls from the
19th century. Like Koganei, he considered these
lesions to be linked with porotic hyperostosis on
the ectocranial surface of the orbits and cranial
vault, and considered them to be of similar
aetiology, i.e. the result of nutritional deficiencies. At this time in Denmark, endocranial lesions
Received 23 September 2002
Revised 6 June 2003
Accepted 23 July 2003
Endocranial Lesions in Non-adult Skeletons

were being recorded by Mller-Christensen
(1961: 63) during his examination of skeletons
from the medieval leprosy hospital at Naestved.
Mller-Christensen referred to the lesions as
cribra cranii interna and again, regarded them as
part of the same process contributing to the
orbital lesions, which he considered inflammatory in origin. It was not until over 10 years later
that endocranial lesions began to be described
more frequently in non-adult remains. Mensforth
et al. (1978) recorded healed and active vascularized periosteal reactions on the endocranial
surfaces in 645 of the Libben children, aged
between 11 months and two years. Mensforth et
al. argued against the lesions being extensions of
porotic hyperostosis from the ectocranial surface
(now thought to result from iron deficiency
anaemia) but instead agreed with Mller-Christensen that they were the result of an inflammatory reaction.
Schultz (1989) found endocranial lesions in up
to 22% of Bronze Age children from five sites in
Central Europe and Anatolia and recorded an
increase in their frequency between the Bronze
Age and medieval period (Schultz, 2001). Schultz
(1989) suggested that skull trauma, resulting in an
epidural haematoma and meningitis, was the
cause of these lesions, and that the increase
may be the result of population growth and
socio-political change (Schultz, 2001). In England, Brothwell & Browne (1994) noted endocranial lesions in eight children between two and 14
years of age from Jewbury in medieval York in
England. They described the lesions as frosted
(remodelled bone projections) and vascularised
(a hyper vascular inner lamina) but no aetiology
was suggested and the bones have since been
reburied.
Despite the increasing interest in these lesions
in the literature, endocranial lesions are not
considered in many core texts on palaeopathology (Aufderheide & Rodriguez-Martin, 1998;
Roberts & Manchester, 1995) and their precise
aetiology is unknown. Schultz (1984, 1993a,
1993b, 1999, 2001) has recorded these lesions
in samples of children and histological analysis is
often employed to try and understand the
mechanism behind their appearance. This
research suggests that hair-on-end lesions,
described by Schultz (1993b) as calcified plaCopyright # 2004 John Wiley & Sons, Ltd.
83
ques on pedicals, represent ossified soft tissue as
the result of inflammation, that fiber bone deposits indicate active bleeding of the meninges and,
that the vascular or capillary type of lesion is
suggestive of healing (Schultz, 1993b). More
recently, Hershkovitz and colleagues (2002)
have suggested that respiratory diseases such as
TB are the most likely cause of these lesions,
which they term Serpens endocrania symmetrics
or SES. This paper explores the possible aetiology of these inflammatory and haemorrhagic
lesions as reported in the literature, and presents
findings on their morphological appearance, distribution and age of occurrence in a group of
children from four cemetery sites in medieval and
post-medieval England.
Development of the skull

The skull develops as three independent areas:
the vault, the base and the facial skeleton. Vault
development is intramembranous and rapid during the first year of life to accommodate the
developing brain, growth slows down around
the seventh year when the vault reaches adult
dimensions. During the first year, the growth of
the vault is achieved by ossification at the margins of the bone, which are covered with an
osteogenic layer. Growth in breadth is achieved
at the sagittal suture and the sutures at the greater
wings of the sphenoid and in height, at the
frontozygomatic suture, pterion, squamosal
suture and the asterion (Williams & Warwick,
1980). By the second year of life the bones of the
sutures have interlocked and growth continues by
bone absorption and deposition at the skull
tables. At birth the cranial vault has one layer,
and the inner and outer lamina (tables) with inner
diploe are not defined until the fourth year.
Around this time the bone begins to thicken,
reaching its maximum at around 35 years.
Growth of the base of the skull occurs mainly
at cartilaginous joints between the sphenoid and
ethmoid, and the sphenoid and occipital bone.
Growth continues, lengthening the skull, at
the spheno-occipital synchondrosis up until the
25th year (Williams & Warwick, 1980). Bone
deposited as the result of appositional growth
in the skeleton involves the deposition of
M. E. Lewis
84
immature, disorganized new bone, which becomes lamellar bone (organised into Haversian
systems) as it matures.
Anatomy of the meninges

Separating the brain from the cranial bones is
a fibrous membrane complex, known as the
meninges. This complex has three layers;
the dura mater, the arachnoid and the pia mater.
The endosteal layer is the internal periosteum for
the cranial bones and contains blood vessels for
their supply. It is attached to the cranial bones,
just as the periosteum is attached to the cortex of
the postcranial bones, and in childhood has
osteogenic capacity (Schultz, 2001). The dura
mater is the outermost and thickest of these
structures and consists of two layers, the endosteal and meningeal (inner) layers. At the margin
of the foramen magnum, the dura mater is continuous with the periosteum lining the vertebral
column (Williams & Warwick, 1980). The middle
layer, the arachnoid, bridges the sulci on the
cortical surface, it has a web-like structure and
lines the inner surface of the dura throughout the
central nervous system. The innermost layer of
the meninges, the pia mater, is the most fragile
layer, turns inwards and provides an intimate

partition between the areas of the brain and the
spinal cord (Agur, 1991). Between the dura and
arachnoid layers is the subdural space into which
haemorrhage may occur. Between the arachnoid
and pia layers is the subarachnoid space, which
only represents a capillary space in the living, and
contains cerebrospinal fluid. Arachnoid granulations are responsible for the absorption of the
cerebrospinal fluids from this central space into
the venous system (Figure 1).
Possible aetiology of endocranial

lesions
Non-specific meningitis
Meningitis is an acute inflammation of the
meninges. The condition has many aetiologies,
both primary and secondary, but usually results
from a bacterial infection in childhood. The most
common pathogens are: Haemophilus influenzae
type b (HIB), Streptococcus pneumoniae and Neisseria
meningitidis often resulting in meningecoccal
meningitis (Rosenthal et al., 1988). Phyogenic
infections may also occur secondary to severe
conditions such as otitis media, syphilis, typhoid
Figure 1. Coronal section through the meninges (after Bradbury,1973: 171).

fever, gastroenteritis, measles, whooping cough,
and pneumonia (Hutchinson & Moncrieff, 1944).
A number of viruses and fungal agents have also
been identified as causative agents and meningitis
may result from tumours or lead poisoning (Patterson, 1993). Childhood infections such as
mumps and measles can also result in neurological involvement. The effect of mumps on the
central nervous system has been noted since 1790
and results in benign meningitis in 10% of all
infections (Kim-Farley, 1993). Meningitis may
involve the dura, referred to as pachymeningitis
or, the arachnoid and pia layers, known as
leptomeningitis.
Pachymeningitis is uncommon in early life but
almost always results from a direct spread of
septic infection from the bones of the skull
secondary to otitis media, mastoiditis or sinusitis.
Pachymeningitis may involve a subdural abscess,
causing thickening and inflammation of the dura
and bone (Cappell & Anderson, 1971: 625). The
poor blood supply of the dura means that haematogenous spread of infection from a distant
site is rare, but when it does occur it is difficult to
treat (McGee et al., 1992). Today, this form of
meningitis is most common as the result of the
spread of pyogenic bacterial from a compound
fracture of the skull (Cappell & Anderson, 1971:
625). Acute bacterial leptomeningitis has a mortality rate today of 20% for pneumnococcal and
510% for meningicoccal infections. In children
under five years of age, infection with H. influenzae
is the most common and has a 510% mortality
rate. In infants, Escherichia coli accounts for 510%
mortality (McGee et al., 1992: 1835). Acute
leptomeningitis usually produces purulent exudate in the subarachnoid space and cerebral
swelling, congestion of the vessels and haemorrhage of the meninges (McGee et al., 1992: 1836).
TB is the most common cause of chronic leptomeningitis, but may affect the dura as the result of
a direct spread of the infection from the petrous
portion of the skull or the spine (Cappell &
Anderson, 1971: 625). Chronic meningitis can
persist for 23 weeks resulting in secondary
hydrocephalus and endarteritis obliterans of the
cerebral arteries.
In his seminal paper, Koganei (1912) describes
the work of several German anatomists who
examined the internal surfaces of the skull at
85
autopsy and described peeling off a layer of
fibrous exudate, superior to a hyperaemic dura,
to reveal a rough skull surface, which Virchow
believed to be the result of a chronic infection
of the skull plates (cited in Koganei, 1912:
120121). More recently, Schultz (1993b) has
argued that endocranial lesions represent vestiges
of the irritation of meninges either from inflammation, trauma, epidural haematoma, a subdural
abscess or tumour, and that inflammation is the
most common cause. Schultz argues that meningitis is followed by increased cerebrospinal pressure, haemorrhage and/or the ossification of
small-grained, scale like soft tissue (Schultz, 1993a:
195). Children with the chronic form of meningitis
in the early 20th century were reported to survive
for a month or even a year and often fell into a
coma before they died (Griffith, 1919). Documentary evidence does suggest that children
could survive for many weeks with a meningeal
infection, long enough to produce new bone
formation. In cases where the child survived for
up to a year, perhaps in a coma, there may be
other skeletal evidence such as osteopenia (or
disuse atrophy), suggestive of paralysis.
Specific meningitis
TB
The spread of Mycobacterium tuberculosis to the
meninges usually occurs during the primary
infection and is, therefore, more common in
young children than adults (Cappell & Anderson,
1971: 630). In 1943, TB was the most frequent
cause of meningitis following a pulmonary or
gastrointestinal infection in England. Common
in the first two years of life, children were
reported to have survived for as long as a week
before falling into a coma and dying 45 days
later (Sheldon, 1943). In 1958, Lorber reported
129 cases of tuberculous meningitis in Sheffield,
where intracranial calcifications and ossifications
occurred between 18 months and three years
after the onset of the disease. However, these
children were receiving treatment for meningitis,
which either cured them or prolonged their life
long enough for lesions to develop. It is not
possible to state whether children could have
survived long enough without treatment in the
86
past to develop calcifications, or if the calcifications Lorber (1958) describes at the base of the
brain relate to the lesions seen on the endocranial
surfaces of the skull. However, Teschler-Nicola
and colleagues (1998) study of 665 skulls from
the Weisbach skeletal collection, Museum of
Natural History in Vienna, found that in 111
cases where the cause of death was recorded as
TB, 73% had corn-size depressions on the endocranial surface, thought to be the result of calcified tubercles in TB meningitis.
Teschler-Nicola (personal communication)
considered the lesions to be indicative of TB
when other signs of the disease accompanied
them on the skeleton. Jankauskas (1999) found
that in early 20th century Vilnius, Lithuania,
granulomatous meningitis was a common complication in children with primary TB, and was
responsible for a third of all clinical forms of the
disease in the pre-antibiotic era. In the 146
children they examined from late medieval to
early modern Alytus, also in Lithuania, Jankauskas
& Schultz (1995) recorded endocranial lesions in
80% (N 116) of non-adults, 16% (N 23) of
which they associated with TB. Closer examination of these lesions at a microscopic level
revealed new bone formation in the base of the
depressions suggestive of healing (Schultz, 1999).
Santos & Roberts (2001) carried out a study on 66
non-adults skeletons from 20th century Portugal,
known to have suffered from TB during life. The
second most common cause of death in these
children was tuberculous meningitis and three of
the sample were documented to have died from
this condition. However, slight endocranial
lesions were only noted on the skeleton of a 19year-old, non-tuberculous female with septicaemia, which would have resulted in rapid death
(Santos & Roberts, 2001: 44).
Most recently, Hershkovitz and co-workers
(2002) noted erosive lesions on the endocranial
surfaces of skulls from the Hamann-Todd collections at the Smithsonian Institution, and reported
them in three of the 40 non-adults (7.5%). They
found the lesions more frequently in non-adults
and in 36% of individuals documented to have
suffered from TB compared to 10% in those who
died of other causes. Hershkovitz and colleagues
(2002) suggest that TB and other respiratory
disorders as the main aetiological factor of these
M. E. Lewis
lesions in ancient populations and after the
17th century, all endocranial lesions are the result
of TB.
In cases of miliary TB leading to meningitis in
childhood, it is unlikely that the postcranial
skeleton will show any signs of the disease, as
this acute infection spreads haematogenously,
from a soft tissue foci in the lung or intestine
(Griffith, 1919). However, hypertrophic osteoarthropathy may be evident in cases where this
initial infection was overcome, as suggested in
the material examined by Santos & Roberts
(2001). Although vascular new bone may be
located endocranially as a result of inflammation
of the dura, research by Lorber (1958), Templin
& Schultz (1994), Teschler-Nicola et al. (1998)
and Jankauskas (1999) suggest that lesions associated with tuberculous meningitis are more
likely in the form of small granulomas (cortical
foci), producing lesions similar to an arachnoid
granulation. This finding has been more recently
supported by the work of Herschkovitz et al.
(2002).
Congenital syphilis
In the secondary stages of venereal syphilis, acute
meningitis occurs in 12% of patients (Lukehart
& Holmes, 1988: 654). Secondary leptomeningitis may be caused by a direct extension of an
infection from gummas on the cranial surface to
the dura, causing erosion of the overlying bone if
confined to the outer surface of the dura (Cappell
& Anderson, 1971: 633). In congenital syphilis,
the base of the skull may be particularly affected,
causing hydrocephalus and distension of the
scalp veins, and spastic paralysis, mental defects,
fits and pituitary disorders can occur (Sheldon,
1943). Cook & Buikstra (1979) identified endocranial lesions in 27% of their Lower Illinois
Valley non-adults and found an association
between these lesions, periostitis, dental defects
and a lower expectation of life. They suggested
meningitis secondary to endemic treponematosis
as a causative factor. There have been several
cases of congenital syphilis published in the
literature, and although there were lesions on
the ectocranial surfaces of the skulls, the presence
of endocranial lesions in these non-adults has
either not been examined, or not recorded

(Ferencz & Jozsa, 1992; Pa`lfi et al., 1992;
Gladykowska-Rzeczycka & Krenz, 1995; Mansilla & Pijoan, 1995; Rothschild & Rothschild,
1997). It is estimated that only 5% of children
with treponemal disease will show evidence of
osseous involvement (Rothschild & Rothschild,
1997) and therefore, endocranial lesions as a
result of these conditions may be rare, but should
continue to be looked for.
Bone tumours
There are several tumours that may affect the
calvarium, but of these only four are commonly
found in children and adolescents; dermoid and
epidermal cysts, monostotic and polystotic
fibrous dysplasia, intramedullary osteosarcoma
and Langerhans cell histiocytosis or histiocytosis
X (Dorfman & Czerniak, 1998). Dermoid and
epidermal cysts can be present at birth and produce
lytic foci with sclerotic margins. These lesions
are unlikely to be confused with the non-specific
osteoblastic hair-on-end lesions, however they
may form a differential diagnosis for the granular
lesions seen in tuberculous meningitis. Fibrous
dysplasia occurs in individuals under the age of
30 years in 70% of cases (Dorfman & Czerniak,
1998). The tumour extends from the diploe and
protrudes into the inner cranium, this bone mass
is different from the more usual endocranial
lesions in its most severe form but, it is unknown
what the early manifestations of this condition
would look like. Both the intramedullary osteosarcoma and Langerhans cell histiocytosis can be distinguished as lytic in nature and usually occur in
individuals under the age of 10 years (Dorfman &
Czerniak, 1998). Given the expression of these
tumours in the cranium, it is doubtful that they
are the main cause of the lesions described so
frequently on the endocranial surfaces of childrens skulls in archaeological samples.
Subdural haematomas
Subdural haematomas occur from the disruption
of delicate bridging veins extending from the
surface of the brain to the dura, with blood and
fluid draining into the sagittal sinus. As blood
87
accumulates within the subdural space, the brain
is displaced adding increasing traction to the
bridging veins which haemorrhage with subsequent trauma (Kleinman, 1987). After the bleeding has ceased, the blood clot is surrounded by a
fibrous, vascularized membrane, which later
becomes detached from the dura, and usually
extends bilaterally to the posterior parietal
region, or to the floor and anterior/middle cranial
fossa (Caffey, 1978). Occasionally, these haematomas may ossify (Kleinman, 1987). Subdural
bleeding is a common and serious lesion in the
first two years of life, resulting from both natal
(birth trauma) and postnatal traumatic events (i.e.
skull trauma in battered baby syndrome). In 1974,
Caffey described subdural and bilateral intraocular bleeding in habitually shaken babies resulting
from whiplash. Caffey (1974) suggested that
intracranial and intraocular bleeding is indicative
of child abuse in these whiplash shaken babies,
when a lack of fractures on the skull and long
bones would ordinarily eliminate child abuse as a
diagnosis. There is also a high incidence of this
condition after purulent meningitis (Caffey,
1978). Cramer & Green (1998) suggest that
over 80% of deaths due to physical abuse occur
in children who are under five years of age and
over 50% are under one year old.
In the early 20th century, death from an
epidural haematoma at childbirth usually
occurred in the first 24h (Griffith, 1919) and
may have resulted from increased and prolonged
pressure on the cranium. Epidural haematomas
usually originate from an arterial source after a
fracture to the skull, and therefore, are often fatal.
However, in cases where there are small bleeds
they are recorded as being indistinguishable from
subdural haematomas (Kleinman, 1987). Extradural haematomas result from skull fractures, with
subsequent separation of the dura from the cranium up to the connective tissue forming the
suture, but may occur without evidence of fracture in children (Cappell & Anderson, 1971).
Nevertheless, the presence of any trauma to the
skull should be noted when recording endocranial lesions. In 1998, Blondiaux and colleagues
reported successive plaque-like deposits on the
endocranial surface of a non-adult skeleton from
4th century Normandy, suspected of having
suffered child abuse.
M. E. Lewis
88
Vitamin deficiencies
In a study carried out on guinea pigs into vitamin
A deficiency, Wolbach & Bessey (1941) reported
growth retardation of the skull, and more interestingly, new bone formation on the parietal
bones of the endocranium, with skull thickening
and bony projections along areas of sinus drainage. Vitamin D deficiency (rickets) has also
been cited as a causative factor resulting in
meningitis (Hutchinson & Moncrieff, 1944),
and was present in the case reported by
Blondiaux and colleagues (1998). Both should
be considered predisposing factors to the cranial
lesions and it is unlikely that, outside of laboratory conditions, an individual will become deficient in only one vitamin. Perhaps one of the
most likely vitamin deficiencies resulting in endocranial lesions is vitamin C.
Vitamin C forms the basis of connective tissues
for the skin, walls of vessels, cartilage and bone,
and it also protects and regulates the biological
processes of other enzymes. Trauma to weakened
meninges as the result of this deficiency may
result in slow haemorrhage stimulating osteoblastic activity. Histological analysis has been
employed to try and distinguish this condition
from anaemic bone reaction on the skull
(Carli-Thiele, 1995). However, in recent analyses
of scurvy lesions of the skulls of children from
Peru and North America, endocranial lesions are
not discussed (Ortner, 1984; Ortner & Ericksen,
1997; Ortner et al., 1999, 2001). It is possible that
trauma to the brain and eyes during child abuse
would also lead to tearing of the fascias lining the
endocranial and orbital surfaces resulting in new
bone formation on the endocranial and orbital
surfaces, just as in scurvy (Roberts & Manchester,
1995: 172). These lesions, in addition to perios-
titis on the arms and legs, may indicate shaken

baby syndrome, and the unilateral nature of
these lesions and accompanying rib fractures
should help distinguish it from the systemic
problems caused by vitamin C deficiency. In
addition, the presence of osteopenia in the long
bones of children with scurvy (Caffey, 1978:
1459) and, if possible, histological sections will
aid diagnosis.
Materials and methods

Five hundred and twenty-eight non-adult skeletons, aged between birth and 17.0 years, from
four contrasting sites in medieval and post-medieval England were examined for evidence of
endocranial lesions. Anglo-Saxon Raunds Furnells in Northamptonshire is the earliest of the
settlements, with a cemetery dating to between
the 10th and 12th centuries. The parish of
St. Helen-on-the-Walls, based in pre-industrial
York (AD 8501550) was contemporaneous with
Wharram Percy, a deserted medieval village in
the Yorkshire Wolds (c. AD 9001500). Finally,
non-adults excavated from the crypt of Christ
Church Spitalfields, in London (AD 17291859)
were chosen to represent the post-medieval
sample (Table 1).
Age-at-death estimates were obtained using
standards of development for the deciduous and
permanent dentition published by Moorrees et al.
(1963a, 1963b) and tabulated by Smith (1991)
and Lewis (1999). Where no teeth were present,
diaphyseal lengths and skeletal maturation were
used to assign an age (Ubelaker, 1989). Age
estimates for fetal and infant remains were
derived from the British standards developed by
Scheuer et al. (1980) based on diaphyseal lengths.
Table1. Site information and number of non-adults included in the study

Site
Raunds Furnells
St. Helen-on-the-Walls
Wharram Percy
Christ Church, Spitalfields
Total
Period (AD)
850^1100
950^1550
950^1500
1729^1859
Context
Total number of
non-adult skeletons
Rural (early medieval)

Urban (later medieval)
Rural (later medieval)
Industrial (post-medieval)
142
200
303
186
831

The skeletons were divided into seven age categories: preterm (<40 lunar weeks), perinate (0)
0.5 years, 0.62.5 years, 2.66.5 years, 6.610.5
years, 10.614.5 years and 14.617.0 years. In
the last age category, individuals were estimated
to be older than 17.0 years when the root of the
third molar was complete (Rc 16.9) but the
89
apex open (Moorrees et al., 1963b). Of the 783
skeletons that could be assigned an age, 528
(67%) had skulls that could be examined for
evidence of endocranial lesions.
Various forms of lesions were identified on the
endocranial surface and divided in to four specific
types (Figures 25):
Figure 2. Porous lesions on the endocranial surface of the occipital in a 40 week old infant (Bournemouth University).
Figure 3. Fiber bone formation on the endocranial surface of the occipital of a childs skull. The vascular impressions are suggestive of
healing (University of Bradford).
90
M. E. Lewis
Figure 4. Capillary lesions on the endocranial surface of the occipital of a childs skull. The vascular impressions extend into the inner lamina and there is no evidence of new bone formation (University of Bradford).
Figure 5. Hair-on-end lesions on the endocranial surface of the occipital of a childs skull.The lesions are an expansion of the diploe and
the frosted appearance is indicative of healing (University of Bradford).
1. pitted lesions (Figure 2);

2. deposits of white or grey, fiber or immature
new bone (Figure 3);
3. capillary formations (new bone organized
with/around vascular structures) (Figure 4);
4. hair-on-end formation (Figure 5).
In some cases, the hair-on-end lesions may

become frosted or thickened and remodelled
(Figure 5). There was no distinction made
between isolated deposits of new bone formation (sometimes referred to as calcified plaques) and the more diffuse lesions, but their
91
Table 2. Percentage of endocranial lesions by site (prevalence)
Site
No.
with skull
No. with
endocranial
lesions
% with
endocranial
lesions
102
92
14
11
13.7
12.0
217
106
33
5
15.2
4.7
517
63
12.2
Raunds Furnells
St. Helen-onthe-Walls
Wharram Percy
Christ Church,
Spitalfields
Total
Figure 6. Eroded defects (arrow) on the endocranial surface indicative of tuberculosis (from Heshkovitz et al., 2002).
general distribution was noted. The lytic lesions

described in TB should be added to these types
(Heshkovitz et al., 2002) (see Figure 6), but
only one case was identified in this study and
so these lesions were omitted from further
analysis. The occurrence of endocranial lesions
within the different age groups was recorded in
addition to their distribution on the internal
surface of the skull, whether confined to the
occipital bone or on the parietals and frontal
bones. Individuals were not included in the study
if the occipital bone was absent and none of the
surviving bones showed any evidence of new
bone formation.
Results
Table 2 gives the number and percentage of
endocranial lesions at each site and Table 3
summarizes the number and percentage of individuals with endocranial lesions in each age
group (Figure 7). In total, 12% of the non-adults
examined had endocranial lesions, with the
majority of the lesions occurring in the 00.5
years (15%) and 0.62.5 year (19%) age categories (Figure 8). Interestingly, the children
interred at Christ Church Spitalfields in industrial
London had a significantly lower prevalence of
the lesions (X2 9.0, P 0.05, d.f. 3) than in
any other group. Although four cases of endocranial lesions were recorded in the older individuals, no children over the age of 14.6 years
displayed endocranial lesions in the sample. At
Raunds Furnells, a child with a dental age of 10.7
years was affected and at St. Helen-on-the-Walls,
a child around 12 years of age had endocranial
lesions. At Wharram Percy, two children around
nine years of age were affected.
In order to try and understand the aetiology of
these lesions, the cases from all the sites were
combined and the type of lesions in each age
category was assessed. The lesions most commonly occurred on the occipital bone (65%) but
were also found on the parietals, frontal and
temporal bones, either in addition to the occipital, or as isolated lesions (Figure 9). In individuals
under six months of age, all cases were porous or
Table 3. Percentage of endocranial lesions by age category

(prevalence)
Age
category
(years)
No.
aged
individuals
No.
with
skull
No. with
endocranial
lesions
% with
endocranial
lesions
0^0.5
0.6^2.5
2.6^6.5
6.6^10.5
10.6^14.5
14.6^17.0
Total
120
233
287
125
48
28
841
79
164
146
79
33
16
517
12
31
14
4
2
0
63
15.2
18.9
9.7
5.0
6.1
0.0
12.2
92
M. E. Lewis
Figure 7. Percentage of endocranial lesions divided by site and age category (prevalence).
Figure 8. Percentage of endocranial lesions in each age category (sites combined).
93
Figure 9. Distribution of lesions (number) on the endocranial surface in each age category (sites combined).
immature new bone lesions and most occurred on

the cruciate eminence of the occipital bone
(82%). However, in the later age groups there
is evidence that vessels were forming in the
immature new bone deposits, and capillary
lesions became more common in the older age
groups suggesting that they may represent healed
lesions. There was no evidence of immature new
bone formation in children over the age of 6.5
years (Figure 10).
In order to ascertain a possible specific aetiology for these lesions, evidence for other conditions was recorded in the non-adult remains. At
Spitalfields, one individual with Potts disease
indicative of TB had isolated lytic foci on the
endocranial surface suggesting tuberculous
meningitis (Burial 2691). Despite the large number of individuals with deficiency diseases at
Spitalfields, endocranial lesions did not appear
to be associated with the condition and in the
total sample, only four of the 64 cases of endocranial lesions (6%) also had evidence of rickets
or scurvy. Although numbers were small, of the
four individuals with head trauma, three of which

were healed, none had evidence of endocranial
lesions.
Discussion and conclusions

The presence of endocranial lesions in non-adult
skeletal remains has been recorded from many
different periods and geographical locations, and
appears to be the result of inflammation or
haemorrhage of the meninges. The exact aetiology of these lesions, however, is still open to
debate and a review of the literature has shown
that trauma, primary and secondary infections of
the meninges, tumours, TB, syphilis and vitamin
deficiencies of A, C and D may all result in
tearing or inflammation of the meninges resulting
in new bone formation. Due to the critical location of the meninges, in such close proximity to
the brain, it has been argued that, if acute
meningitis occurred, the child would die so
rapidly that there would be no time for new
M. E. Lewis
94
Figure 10. Type of lesion (percent) on the endocranial surface in each age category (sites combined).
bone formation to occur. Texts from the early

20th century have shown children to survive with
chronic meningitis (including tuberculous and
syphilitic infections) for days and weeks and
may survive for several more weeks once descending into a coma. In addition, Wolffs law
dictates that bone remodels in response to external stresses and strains, and therefore, in the
growing child, this response is more pronounced
than in an adult whose bone is remodelling at a
comparatively slower rate (Jones, 1998). Paediatric bone is more vascular and will, therefore,
respond more readily to hyperaemic or inflammatory stimuli. In the first year of a childs life,
there is a rapid turnover of the skeleton, which
decreases in adulthood to a turnover of 5% for
compact, and 25% for cancellous bone (Scheuer
& Black, 2000). If it is considered that in
adult bone osteoblasts take 10 times longer to
replace the bone removed by osteoclasts, then
this time should be reduced when considering
the developing skeletons response time to
inflammation or trauma, and the production of
new bone.
One of the limitations of non-adult palaeopathology is the fact that fiber bone deposited as
part of the growth process, is indistinguishable
from that which may occur as the result of
inflammation or haemorrhage in a disease process. Therefore, bone laid down by the osteogenic dura during childhood may be part of the
normal growth process that is occurring rapidly
in the first two years of life. The majority of bone
lesions deposited in the youngest age categories
in the current study were characterized as diffuse
layers of fiber bone, mostly on the occipital
surface, surrounding the cruciate eminence.
Only in the later age categories did capillary
and hair-on-end lesions also occur, and then
the lesions were also more widespread. This
suggests that the majority of cases in the youngest age category (00.5 years) were probably
non-pathological in origin, and the result of rapid
growth in that area. However, intra-cranial haemorrhage can occur in preterm infants as a result
of mineral deficiency during this rapid growth
period (Seow, 1992). A more widespread deposit
is probably indicative of pathology and occurred

in the older age groups with 66% of the 24 cases
in the 0.62.5 year age category also having
lesions on the parietals, frontal and temporal
bones. The results also suggests that lesions
showing vascular impressions, whether extending
into the inner lamina or within fiber bone formations represent healed lesions and these were
more commonly found in the older individuals
in the English samples.
In order to understand the aetiology of these
lesions, researchers need to record the distribution, type and ages of individuals affected in
addition to other skeletal lesions that may suggest a specific pathology. For instance, haemorrhage of torn meninges may be the result of
child abuse and could be found in association
with head trauma or rib fractures, or as the result
of scurvy, identified by new bone formation/
apposition and pitted lesions on the sphenoid,
mandibular ramus and maxilla (Ortner & Ericksen, 1997). The exact aetiology of each type of
lesion is still difficult to distinguish, however,
histological evidence does suggest that hair-onend lesions are the result of inflammation perhaps
secondary to infection, whereas new bone formation results from haemorrhage. Only in the
case of TB are there specific corn-sized granular
lesions, however, they must not be confused with
normal arachnoid granulations, which are
uncommon in non-adults.
Contrary to Schultzs (2001) study of European populations, the children from Christ
Church Spitalfields showed fewer lesions than
their peers from early and later medieval England,
and lesions only occurred in the ages of six
months and 6.5 years. The majority of these
lesions were fiber bone on the occipital and
may have represented growth deposits. The reason for the paucity of evidence in this sample is
not known, and is surprising considering the high
prevalence of deficiency diseases in this industrial
sample, suggesting that haemorrhage of the
meninges as the result of vitamin C deficiency
may be a rare cause of the lesions. Until the
precise aetiology of these lesions can be ascertained, they should be referred to as non-specific
indicators of haemorrhage or infection and population studies on large non-adult samples from
different periods in Europe and North America
need to be carried out.
95
Acknowledgements
This research was, in part, funded by a University
of Bradford Research Studentship. I thank Louise
Humphrey (Natural History Museum, London),
Simon Mays (English Heritage) and Elizabeth
Hartley (Yorkshire Museum) for access to the
collections. Thanks also go to Dr Maria TeschlerNicola (Natural History Museum, Vienna)
for her information on the TB lesions, and the
two anonymous reviews for their valuable
comments.
References
Agur AMG. 1991. Grants Atlas of Anatomy. Williams
and Wilkins: Baltimore.
Aufderheide AC, Rodriguez-Martin C. 1998. The Cambridge Encyclopedia of Human Paleopathology. Cambridge University Press: Cambridge.
Blondiaux G, Blondiaux J, Secousse F, Cotton A,
Danze P-M, Flipo R-M. 1998. Rickets and child
abuse: the case of a 4th century girl from Normandy. Proceedings of XIIth European Meeting of the
Paleopathology Association. SPA Teramo: Italy; 15.
Bradbury S. 1973. Hewers Textbook of Histology for
Medical Students, 9th edition. William Heinemann
Medical Books Ltd: London.
Brothwell D, Browne S. 1994. Pathology. In The Jewish
Burial Ground at Jewbury, Lilley SM, Stroud G,
Brothwell DR, Williamson MH (eds). Current British Archaeology: York; 465466.
Caffey J. 1974. The whiplash shaken infant
syndrome: manual shaking by the extremities with
whiplash-induced intracranial and intraocular
bleedings, linked with residual permanent brain
damage and mental retardation. Pediatrics 54(4):
396403.
Caffey J. 1978. Pediatric X-Ray Diagnosis. Tear Book
Medical Publishers, Inc.: Chicago.
Cappell DF, Anderson JR. 1971. Muirs Textbook of
Pathology. Edward Arnold: Chicago.
Carli-Thiele P. 1995. Scurvy: investigations on the
human skeleton using macroscopic and microscopic, radiological methods. Journal of Paleopathology 7: 88.
Cook DC, Buikstra JE. 1979. Health and differential
survival in prehistoric populations: prenatal dental
defects. American Journal of Physical Anthropology 51:
649664.
Cramer KE, Green NE. 1998. Child abuse. In Skeletal
Trauma in Children, Volume 3, Green NE,
96
Swiontkowski MF (eds). W.B. Saunders Company:
Philadelphia; 577594.
Dorfman HD, Czerniak B. 1998. Bone Tumors. Mosby:
London.
Ferencz M, Jozsa L. 1992. Congenital syphilis on a
medieval skeleton. Anthropologie 30(1): 9598.
Gladykowska-Rzaczycka JJ, Krenz M. 1995. Extensive
change within a subadult skeleton from a medieval
cemetery of Slaboszewo, Mogilno District, Poland.
Journal of Paleopathology 3: 177184.
Griffith JPC. 1919. The Diseases of Infants and Children.
W.B. Saunders and Company: London.
Henschen F. 1961. Cribra cranii, a skull condition said
to be of racial or geographical nature. Pathological
Microbiology 24: 724729.
Hershkovitz I, Greenwald CM, Latimer B, Jellema
SW-B, Eshed V, Dutour O, Rothschild BM. 2002.
Serpens Endocrania Symmetrica (SES): a new term
and a possible clue for identifying intrathoracic
diseases in skeletal populations. American Journal of
Physical Anthropology 118(3): 201216.
Hutchinson R, Moncrieff A. 1944. Lectures on Diseases of
Children. Edward Arnold and Co.: London.
Jankauskas R. 1999. Tuberculosis in Lithuania: paleopathological and historical correlations. In Tuberculosis: Past and Present, Palfi G, Dutour O, Deak J,
Hutas I (eds). Golden Book Publisher Ltd., Tuberculosis Foundation: Szeged; 551558.
Jankauskas R, Schultz M. 1995. Meningeal reactions in
a late medieval-early modern child population from
Alytus, Lithuania. Journal of Paleopathology 7(2): 106.
Jones E. 1998. Skeletal growth and development as
related to trauma. In Skeletal Trauma in Children, Green
NE, Swiontkowski MF (eds). W.B. Saunders Company: Philadelphia; 116.
Kim-Farley RJ. 1993. Mumps. In The Cambridge World
History of Human Disease, Kiple K (ed.). Cambridge
University Press: Cambridge; 887889.
Kleinman PK. 1987. Skeletal trauma: general considerations. In Diagnostic Imaging of Child Abuse, Kleinman PK (ed.). Williams and Wilkin: Baltimore;
527.
Koganei H. 1912. Cribra cranii und cribra orbitalia.
Mitt Med Fak Toyko 10: 113154.
Kreutz K, Teichmann G, Schultz M. 1995. Palaeoepidemiology of inflammatory processes of the skull:
a comparative study of two early medieval infant
populations. Journal of Paleopathology 7(2): 108.
Lewis ME. 1999. The Impact of Urbanization and Industrialization in Medieval and Post-medieval Britain. An
Assessment of the Morbidity and Mortality of Non-adult
Skeletons from the Cemeteries of Two Urban and Two Rural
Sites in England (AD 8501859). Ph.D. thesis. University of Bradford.
M. E. Lewis
Lukehart SA, Holmes KK. 1988. Syphilis. In Harrisons
Principles of Internal Medicine, Wilson JD, Braunwald E,
Isselbacher KJ, Petersdorf RG, Martin JB, Fauci AS,
Root RK (eds). McGraw-Hill Inc.: New York; 651
663.
Lorber J. 1958. Intracranial calcifications following
tuberculosis meningitis in children. Acta Radiololgy
50: 204210.
Mansilla J, Pijoan CM. 1995. Brief communication: a
case of congenital syphilis during the Colonial
period in Mexico City. American Journal of Physical
Anthropology 97: 187195.
McGee JOD, Isaacson PG, Wright NA. 1992. Oxford
Textbook of Pathology. Oxford University Press:
Oxford.
Mensforth RP, Lovejoy OC, Lallo JW, Armelagos GJ.
1978. The role of constitutional factors, diet and
infectious disease in the etiology of porotic hyperostosis and periosteal reactions in prehistoric infants and children. Medical Anthropology 2: 159.
Mller-Christensen V. 1961. Bone Changes in Leprosy.
Munksgaard: Copenhagen.
Moorrees CFA, Fanning EA, Hunt EE. 1963a. Formation and resorption of three deciduous teeth in
children. American Journal of Physical Anthropology
21: 205213.
Moorrees CFA, Fanning EA, Hunt EE. 1963b. Age
variation of formation stages for ten permanent
teeth. Journal of Dental Research 42: 14901502.
Ortner DJ. 1984. Bone lesions in a probable case of
scurvy from Metlatavik, Alaska. MASCA Journal 3:
7981.
Ortner DJ, Ericksen MF. 1997. Bone changes in the
human skull probably resulting from scurvy in
infancy and childhood. International Journal of Osteoarchaeology 7: 212220.
Ortner DJ, Kimmerle EH, Diez M. 1999. Evidence of
scurvy in subadults from archaeological sites in
Peru. American Journal of Physical Anthropology 108:
321331.
Ortner DJ, Butler W, Cafarella J, Milligan L. 2001.
Evidence of probable scurvy in subadults from
archaeological sites in North America. American
Journal of Physical Anthropology 114: 343351.
Pa`lfi G, Dutour O, Borreani M, Brun J-P, Berato J.
1992. Pre-Columbian congenital syphilis from the
late antiquity in France. International Journal of Osteoarchaeology 2: 245261.
Patterson KD. 1993. Meningitis. In The Cambridge
World History of Human Disease, Kiple K (ed.). Cambridge University Press: Cambridge; 875880.
Roberts C, Manchester K. 1995. The Archaeology of
Disease, 2nd edition. Alan Sutton Publishing Limited: Gloucester.

Rosenthal J, Dagan R, Press J, Sofer S. 1988.
Differences in the epidemiology of childhood
community-acquired bacterial meningitis between two ethnic populations cohabiting in one
geographical area. Paediatric Infectious Disease Journal
7: 630633.
Rothschild BM, Rothschild C. 1997. Congenital syphilis in the archaeological record: diagnostic insensitivity of osseous lesions. International Journal of
Osteoarchaeology 7: 3942.
Santos AL, Roberts CA. 2001. A picture of tuberculosis in young Portuguese people in the early 20th
century: a multidisciplinary study of the skeletal
historical evidence. American Journal of Physical
Anthropology 115(1): 3849.
Scheuer JL, Musgrave JH, Evans SP. 1980. The
estimation of late fetal and perinatal age from
limb bone length by linear and logarithmic regression. Annals of Human Biology 7: 257265.
Scheuer L, Black S. 2000. Developmental Juvenile Osteology. Academic Press: London.
Schultz M. 1984. The diseases in a series of
childrens skeletons from Ikiz Tepe, Turkey. In
Proceedings of the Fifth European Meeting of the Palaeopathology Association, Siena, Italy, Capecchi V,
Rabino Massa E (eds). Tipografia Senese: Siena;
321325.
Schultz M. 1989. Causes and frequency of diseases
during early childhood in Bronze Age populations.
In Advances in Palaepathology, Capasso L (ed.). Marino
Solfanelli Editore: Chieti; 175179.
Schultz M. 1993a. Initial stages of systemic bone
disease. In Histology of Ancient Human Bone: Methods
and Diagnosis, Grupe G, Garland AN (eds). SpringerVerlag Inc.: New York; 185203.
97
Schultz M. 1993b. Vestiges of Non-Specific Inflammation in
Prehistoric and Historic Skulls: A Contribution to Palaeopathology. Anthropolgische Beitrage: Aesch.
Schultz M. 1999. The role of tuberculosis in infancy
and childhood in prehistoric and historic populations. In Tuberculosis: Past and Present, Palfi G, Dutour
O, Deak J, Hutas I (eds). Golden Book Publisher
Ltd., Tuberculosis Foundation: Szeged; 503507.
Schultz M. 2001. Paleohistopathology of bone: a new
approach to the study of ancient diseases. Yearbook
of Physical Anthropology 44: 106147.
Seow KW. 1992. Dental enamel defects in low birth
weight children. Journal of Paleopathology, Monographic Publication 2: 321330.
Sheldon W. 1943. Diseases of Infancy and Childhood. J.
and A. Churchill Ltd.: London.
Smith BH. 1991. Standards of human tooth formation
and dental age assessment. In Advances in Dental
Anthropology, Kelley MA, Larsen CS (eds). WileyLiss, Inc.: New York; 143168.
Templin O, Schultz M. 1994. Evidence of tuberculosis
in the medieval infant population from Bettinger
(Switzerland). HOMOJournal of Comparative Human Biology 45: S130.
Teschler-Nicola M, Gerold F, Prodinger W. 1998.
Endocranial features in tuberculosis. Proceedings of the
XIIth European Meeting of the Palaeopathology Association.
SPA Teramo: Italy; 92.
Ubelaker DH. 1989. Human Skeletal Remains. Excavation,
Analysis, Interpretation. Taraxacum: Washington.
Williams PL, Warwick R. 1980. Grays Anatomy.
Churchill Livingstone: Edinburgh.
Wolbach SB, Bessey OA. 1941. Vitamin A deficiency
and the nervous system. Archives of Pathology 32(5):
689722.

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Int. J. Osteoarchaeol. 14: 8297 (2004)