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Fast Facts: Multiple Sclerosis
First published 2000; second edition 2006; third edition 2014; fourth edition 2016
Fifth edition 2021

Text © 2021 Stella E Hughes, Gabrielle Macaron

© 2021 in this edition S. Karger Publishers Ltd

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Abingdon, Oxford OX14 3LN, UK
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All rights reserved. No part of this publication may be reproduced, stored in a

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The rights of Stella E Hughes and Gabrielle Macaron to be identified as the authors
of this work have been asserted in accordance with the Copyright, Designs &
Patents Act 1988 Sections 77 and 78.

The publisher and the authors have made every effort to ensure the accuracy of
this book, but cannot accept responsibility for any errors or omissions.

For all drugs, please consult the product labeling approved in your country for
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Registered names, trademarks, etc. used in this book, even when not marked as
such, are not to be considered unprotected by law.

A CIP record for this title is available from the British Library.

ISBN 978-3-318-06797-2
Hughes SE (Stella)
Fast Facts: Multiple Sclerosis/
Stella E Hughes, Gabrielle Macaron

Medical illustrations by Annamaria Dutto, Withernsea, UK.

Typesetting by Amnet, Chennai, India.
Printed in the UK with Xpedient Print.
Contents

List of abbreviations

Introduction

Epidemiology and genetics

Pathology

The clinical picture

Treatment of relapses and symptoms

Disease-modifying treatment

Emerging therapies

Special MS populations

Lifestyle considerations and the multidisciplinary team

Advanced MS

Useful resources

Index
List of abbreviations

9-HPT: 9-hole peg test

AAN: American Academy of Neurology
ACTH: adrenocorticotropic hormone
ADEM: acute disseminated encephalomyelitis
ADL: activities of daily living
AHSCT: autologous hematopoietic stem cell transplantation
AQP-4: aquaporin 4
bd: twice daily
CIS: clinically isolated syndrome
CNS: central nervous system
CSF: cerebrospinal fluid
CT: computed tomography
DHODH: dihydroorotate dehydrogenase
DIS: dissemination in space
DIT: dissemination in time
DMT: disease-modifying therapy
EAN: European Academy of Neurology
EBV: Epstein–Barr virus
ECTRIMS: European Committee of Treatment and Research in Multiple Sclerosis
EDSS: Expanded Disability Status Scale
EMA: European Medicines Agency
FDA: (US) Food and Drug Administration
FLAIR: fluid-attenuated inversion recovery
HLA: human leukocyte antigen
IFN-β: interferon-beta
IgG: immunoglobulin G
IL: interleukin
INO: internuclear ophthalmoplegia
IPMSSG: International Pediatric Multiple Sclerosis Study Group
i.v.: intravenous
JC: John Cunningham (virus)
MHC: major histocompatibility complex
MOG: myelin oligodendrocyte glycoprotein
MRI: magnetic resonance imaging
MS: multiple sclerosis
MSFC: Multiple Sclerosis Functional Composite
MSN: multiple sclerosis specialist nurse
NEDA: no evidence of disease activity
NMO: neuromyelitis optica
NMOSD: neuromyelitis optica spectrum disorder
Nrf2: nuclear factor (erythroid-derived 2)-like 2
PCR: polymerase chain reaction
PEG: percutaneous enteral gastrostomy
PLEX: plasma exchange
PML: progressive multifocal leukoencephalopathy
POMS: pediatric-onset multiple sclerosis
PPMS: primary progressive multiple sclerosis
PRMS: progressive relapsing multiple sclerosis
RCT: randomized controlled trial
RIS: radiologically isolated syndrome
RRMS: relapsing remitting multiple sclerosis
S1P: sphingosine 1-phosphate
SDMT: Symbol Digit Modalities Test
SLE: systemic lupus erythematosus
SNRI: serotonin–norepinephrine reuptake inhibitor
SPMS: secondary progressive multiple sclerosis
STIR: short time inversion recovery
T25FW: timed 25-foot walk
TKI: tyrosine kinase inhibitor
TNF: tumor necrosis factor
UTI: urinary tract infection
UV: ultraviolet (light)
VCAM1: vascular cell adhesion molecule-1
WHO: World Health Organization
Introduction

Multiple sclerosis (MS) is a leading cause of disability in young

adults, and it has a significant effect on patients’ quality of life,
family plans and careers. By causing varying degrees of physical and
cognitive disability, MS carries a considerable individual and societal
economic burden.
Fortunately, we are entering a new era in the management of MS.
Several recent studies support initiating treatment early in the
disease course with higher-efficacy disease-modifying therapies in
patients with relapsing-remitting MS. This approach has been
associated with better long-term outcomes, specifically a lower risk
of conversion to secondary progressive MS. Moreover, new molecules
with the potential to induce myelin repair or halt the
neurodegenerative process are in the pipeline for the treatment of
progressive MS. Coupled with a recent update to the diagnostic
criteria, clinicians can now diagnose and treat patients in the earliest
phases of their disease.
In this new edition of Fast Facts: Multiple Sclerosis, we present
the latest evidence on disease pathogenesis and all clinical aspects
of the condition, as well as the latest on disease-modifying therapies
and other potential treatments.
Given the need for multidisciplinary management of MS, we have
written this resource for the benefit of all health professionals
involved in the care of patients with this complex disease.

Acknowledgments. The authors wish to thank the authors of the

third and fourth editions of this resource, Drs Michael Barnett, Omar
Malik, Ann Donnelly, Mary Rensel and Orla Gray, for the strong
foundation on which this new edition is based.
 1 Epidemiology and genetics

Multiple sclerosis (MS) is a neurological condition resulting from

inflammation and degeneration within the central nervous system
(CNS). This inflammation can affect different sites at different times,
producing a variety of symptoms and signs. Periods of relapse and
remission occur in the early stages of the disease, and in most
patients a slowly progressive course ensues within one to two
decades of disease onset. The cause of MS is unknown, but
dysregulation of the immune system is central to the pathogenesis
of the disease.
Epidemiology
MS is the leading cause of neurological disability in the young and
middle-aged populations of the developed world. Survey figures from
2020 suggest that it affects 2.8 million people worldwide.1 Given the
lack of complete surveillance data in some countries, this is likely to
be an underestimate.

Prevalence. The worldwide prevalence of MS appears to be

increasing. This is related to many factors, including improved
counting methods, better diagnosis, global population growth,
people with MS living longer (through improved treatment and
support) and a true increase in disease incidence, especially in
females.
The number of people with MS in a given population at any one
time is usually expressed as cases per 100 000 population.
Prevalence varies worldwide, but MS is most prevalent in northern
European populations, especially in individuals of Nordic descent,
and is notably more prevalent in temperate than equatorial regions.
While, globally, the median estimated prevalence of MS is 36 per 100
000,1 in some countries, prevalence exceeds 300 per 100 000.
Regionally, the median estimated prevalence of MS is greatest in
Europe and the Americas (133 and 112 per 100 000, respectively).1
However, prevalence varies significantly both within regions and
within countries. For example, in Europe, San Marino and Germany
have the highest prevalence of MS in the world (337 and 303 per
100 000, respectively), whereas some European countries have
prevalence figures below 40 per 100 000.1
In the Global Burden of Disease Study 2016, the highest age-
standardized MS prevalence estimates (given as per 100 000
population) were in high-income North America (164.6), western
Europe (127.0) and Australasia (91.1), and the lowest were in
eastern and central sub-Saharan Africa (3.3 and 2.8, respectively)
and Oceania (2.0).2
Incidence. The number of new cases per 100 000 population per
year can indicate changes in the risk of a disease within a
population, and can signify whether the disease frequency is
increasing in a population. It is not affected by changes in survival.
The incidence of MS, which peaks at age 30, appears to be rising in
both the northern and southern hemispheres, particularly in women.
The median estimated global incidence of MS is 2.5 per 100 000 per
year, but in some countries the incidence may exceed 10 per 100
000 per year.3

Geo-epidemiology of MS. The prevalence of MS is significantly

associated with latitude, particularly in populations of European
descent (Figure 1.1). The ‘latitudinal gradient’ in MS has been
confirmed by independent studies in Australia, New Zealand and the
USA, with exceptions in Sardinia and northern Scandinavia.4 In
Australia, the age-standardized prevalence is highest in Tasmania,
almost double that in Queensland.5 Genetic variation between
geographically discrete populations has been invoked as one
explanation for this observation, particularly within the human
leukocyte antigen (HLA). However, a statistically significant
relationship between MS prevalence and latitude persists in some
European populations even after adjustment for HLA-DRB1 allele
frequency,4 supporting a role for environmental factors that vary
with latitude, such as ultraviolet (UV) light exposure, viral infections
and vitamin D levels.

Sex. MS is more common in women than men, at a ratio of 2–3:1.

In Denmark, where an MS registry has been ongoing since 1950, the
incidence of MS has doubled in women, but has increased by only
24% in men.6 An increasing incidence in females only has been
observed in several other northern hemisphere countries, including
Canada,7 Finland8 and Japan.9 An exploratory analysis across
different geographic areas worldwide also showed a latitudinal
gradient to the increased sex ratio.10 The pediatric MS population
has a prepubertal sex ratio of 1:1, pointing to a likely association
between sex hormones and disease onset.11

Figure 1.1 Geographic distribution of MS, showing a greater

prevalence at high latitudes. Source: Atlas of MS, 3rd edition.
Multiple Sclerosis International Federation, 2020.1

Environmental risk factors include:

• UV radiation and season of birth
• levels of dietary vitamin D
• Epstein–Barr virus (EBV) infection
• smoking
• migration.
 Ultraviolet radiation and season of birth. The latitudinal
prevalence gradient for MS may be explained in part by a
relationship to exposure to UV radiation from sunlight, as there is an
association between low levels of UVB exposure and development of
MS. This may explain the ‘season of birth effect’ whereby those born
in spring (April) in countries in the northern hemisphere have a
significantly higher relative risk of developing MS than those born in
winter months (October).12 This may be related to maternal
exposure to UV light.
Dietary vitamin D. There is an association between low levels
of vitamin D and a number of diseases, including MS. Diet, dietary
supplements and ambient UV exposure are all sources of vitamin D.
Populations exposed to limited sunlight but who consume diets rich
in fatty fish (a good source of vitamin D) have lower MS prevalence
rates than expected for their latitude.13 Prospective studies have
shown that MS risk is lower in groups who take vitamin D
supplements regularly.14 Higher vitamin D levels are associated with
lower risk of relapse15 and slower rates of progression in MS. Studies
in patients with clinically isolated syndromes have reported a delay
before the second inflammatory episode in people with higher
vitamin D levels.16,17
Epstein–Barr virus is a double-stranded DNA virus that is
transmitted via saliva. EBV does not always cause illness, and early
childhood infection with the virus is usually asymptomatic. The acute
illness caused by EBV, infectious mononucleosis, often accompanies
primary infection in adolescence or young adulthood. Individuals
with MS are rarely seronegative for EBV, and there is a strong
association between previous history of infectious mononucleosis
and MS, with a twofold greater risk of MS in this group.18 There also
appears to be a relationship between the titers of EBV
immunoglobulin G (IgG) and the risk of MS.19 The nature of the
association between EBV and MS is yet to be established, but the
infection may trigger or potentiate autoimmunity.
Smoking. The relative risk of developing MS is around 1.5 times
higher for smokers than non-smokers,20 and there is a direct link
between duration and intensity of smoking. Cultural trends that have
led to an increase in the number of female smokers may be
contributing to the rising incidence of MS in females (see page 10).
However, the risk appears to be greater in male (threefold) than
female (twofold) smokers. The risk of developing secondary
progressive MS (see page 30) is higher in ‘ever smokers’ than ‘never
smokers’.20
Migration studies support a relationship between the country of
origin and risk of MS. An individual’s age at the time of migration
from a high-prevalence area to one of low prevalence appears to
affect the risk for MS, with a critical time period that may extend into
early adulthood.21 Although this observation lends indirect support to
the hypothesis that environmental factors contribute to MS risk, the
correlation between migration and MS risk is not necessarily
maintained when people from communities that do not classically
have a high MS prevalence, such as the Japanese, move to areas of
high prevalence.21

Ethnicity. MS is more common in people with northern European

ancestry. The incidence is lower in people of Asian/African or South
American heritage.22 People of different ethnicities living in the same
environment have different prevalence rates for MS. For example, in
the UK, the prevalence of MS was found to be considerably lower in
black (African or Caribbean descent) and south Asian (Indian,
Bangladeshi, Pakistani or Sri Lankan descent) people living in east
London than in white (British, American or European descent)
people living in the same area. However, MS is several times more
prevalent in black and south Asian people living in the UK than in
those living in Africa and south Asia (although the data from less-
developed countries are limited).23 These findings highlight both the
genetic contribution to MS susceptibility and the effect of
environmental factors on MS risk.
Genetics
No single causative gene for MS has been identified. However,
people with a family member with MS have a greater risk of
developing the disease (Table 1.1).24 Concordance between female
monozygotic (identical) twins approaches 40%, while dizygotic (non-
identical) twins have a concordance rate of approximately 4% and
non-twin siblings have a relative risk 15–20 times that of the local
population.25 Although these figures also implicate environmental
factors in the genesis of MS, studies of ‘non-biological siblings’, that
is, siblings who share the same environment but have different
biological parents, do not suggest an increased risk related solely to
environment. It is therefore likely that an individual’s genetic
background modulates susceptibility to environmental risk factors.

TABLE 1.1
Population-based prevalence in relatives of a person with
MS

1/1000
General population
1/1000
Adoptive siblings 7/1000
First cousin 13/1000
21/1000
Paternal half sibling
24/1000
Half sibling reared apart 35/1000
Maternal half sibling 80/1000
90/1000
Full sibling
197/1000
HLA-identical sibling 200/1000
Sibling in consanguineous mating* 270/1000
 Child of sibling
Offspring of conjugal pair
Monozygotic twin
*
Sibling with the same parents, where the parents are related.
Adapted from Ebers 2008.24

There is a strong association between susceptibility to MS and

specific HLA alleles that code for major histocompatibility complex
(MHC) class II antigens. These antigens are expressed on antigen-
presenting cells (including dendritic cells, macrophages and B
lymphocytes). In northern Europeans, the HLA-DRB1*1501 allele
(and HLA-DR15 haplotype) has shown a consistent association with
MS and is said to increase the risk of MS threefold.26 It may be that
an effect of one gene is modified by several other genes (epistasis).
Furthermore, epigenetic modulation of the MHC by environmental
factors such as vitamin D, smoking, EBV infection and early-life
hygiene may modify the effect of allelic variation at this site.
A number of other susceptibility loci have been identified; in a
study of over 14 000 people with MS, the International Multiple
Sclerosis Genetics Consortium expanded the number of genetic
variations associated with MS to more than 100.27 Most of the risk
alleles associated with MS are related to function of the immune
system. However, only around 25% of the disease heritability is
explained by the MS risk loci identified to date.26
An individual’s genetic background may also explain the varied
response to immunotherapy. Pharmacogenomic studies are ongoing.

Key points – epidemiology and genetics

 • At least 2.3 million people worldwide have been diagnosed
with MS.
• MS is more common in women than men (2–3:1), and the
incidence of MS in females is rising.
• The prevalence of MS is increasing worldwide, with a
greater prevalence in populations of northern European
descent.
• MS has a ‘latitudinal gradient’, that is, a higher prevalence
and incidence of MS in areas of higher latitude (remote
from the equator).
• There is an association between low levels of vitamin D
and prevalence (and possibly severity) of MS.
• Most people with MS have been exposed to EBV. People
who have had infectious mononucleosis have a twofold
higher risk of developing MS.
• Smokers are around 1.5 times more likely to develop MS
than non-smokers.
• MS has a heritable component, but the condition is not
related to a single gene (multiple gene interactions are
likely to be involved); the HLA allele DRB1*1501 (and HLA-
DR15 haplotype) has a strong association with MS in
people of northern European descent.

Key references
1. MSIF. Atlas of MS 2020: Mapping Multiple Sclerosis Around The World. Key Epidemiology Findings.
Multiple Sclerosis International Federation, 2020. www.msif.org/wp-content/uploads/2020/10/Atlas-3rd-
Edition-Epidemiology-report-EN-updated-30-9-20.pdf, last accessed 15 October 2020.
2. GBD 2016 Neurology Collaborators. Global, regional, and national burden of neurological disorders,
1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol
2019;18:459–80.
3. WHO. Atlas. Multiple Sclerosis Resources in the World. World Health Organization, 2008.
www.who.int/mental_health/neurology/Atlas_MS_WEB.pdf, last accessed 12 August 2020.
4. Simpson S Jr, Blizzard L, Otahal P et al. Latitude is significantly associated with the prevalence of
multiple sclerosis: a meta-analysis. J Neurol Neurosurg Psychiatry 2011;82:1132–41.

5. Campbell JA, Simpson S Jr, Ahmad H et al. Change in multiple sclerosis prevalence over time in
Australia 2010–2017 utilising disease-modifying therapy prescription data. Mult Scler 2020;26:1315–28.
6. Koch-Henriksen N, Thygesen LC, Stenager E et al. Incidence of MS has increased markedly over six
decades in Denmark particularly with late onset and in women. Neurology 2018;90:e1954–63.
7. Orton S-M, Herrera BM, Yee IM et al. Sex ratio of multiple sclerosis in Canada: a longitudinal study.
Lancet Neurol 2006;5:932–6.
8. Krökki O, Bloigu R, Reunanen M, Remes AM. Increasing incidence of multiple sclerosis in women in
Northern Finland. Mult Scler 2011;17:133–8.

9. Osoegawa M, Kira J, Fukazawa T et al. Temporal changes and geographical differences in multiple
sclerosis phenotypes in Japanese: nationwide survey results over 30 years. Mult Scler 2009;15:159–73.
10. Trojano M, Lucchese G, Graziano G et al. Geographical variations in sex ratio trends over time in
multiple sclerosis. PLoS One 2012;7:e48078.
11. Chabas D, Green AJ, Waubant E. Pediatric multiple sclerosis. NeuroRx 2006;3:264–75.

12. Dobson R, Giovannoni G, Ramagopalan S. The month of birth effect in multiple sclerosis: systematic
review, meta-analysis and effect of latitude. J Neurol Neurosurg Psychiatry 2013;84:427–32.
13. Bäärnhielm M, Olsson T, Alfredsson L. Fatty fish intake is associated with decreased occurrence of
multiple sclerosis. Mult Scler 2014;20:726–32.
14. Munger KL, Zhang SM, O’Reilly E et al. Vitamin D intake and incidence of multiple sclerosis.
Neurology 2004;62:60–5.
15. Simpson S Jr, Taylor B, Blizzard L et al. Higher 25-hydroxyvitamin D is associated with lower relapse
risk in multiple sclerosis. Ann Neurol 2010;68:193–203.
16. Martinelli V, Dalla Costa G, Colombo B et al. Vitamin D levels and risk of multiple sclerosis in patients
with clinically isolated syndromes. Mult Scler 2014;20:147–55.
17. Ascherio A, Munger KL, White R et al. Vitamin D as an early predictor of multiple sclerosis activity
and progression. JAMA Neurol 2014;71:306–14.

18. Thacker EL, Mirzaei F, Ascherio A. Infectious mononucleosis and risk for multiple sclerosis: a meta-
analysis. Ann Neurol 2006;59:499–503.

19. Ascherio A, Munger KL, Lennette ET et al. Epstein–Barr virus antibodies and risk of multiple sclerosis:
a prospective study. JAMA 2001;286:3083–8.
20. Wingerchuk DM. Smoking: effects on multiple sclerosis susceptibility and disease progression. Ther
Adv Neurol Disord 2012;5:13–22.
21. Gale CR, Martyn CN. Migrant studies in multiple sclerosis. Prog Neurobiol 1995;47:425–48.
22. Koch-Henriksen N, Sørensen PS. The changing demographic pattern of multiple sclerosis
epidemiology. Lancet Neurol 2010;9:520–32.
23. Albor C, du Sautoy T, Kali Vanan N et al. Ethnicity and prevalence of multiple sclerosis in east
London. Mult Scler 2017;23:36–42.

24. Ebers GC. Environmental factors and multiple sclerosis. Lancet Neurol 2008;7:268–77.
25. Dyment DA, Ebers GC, Sadovnick AD. Genetics of multiple sclerosis. Lancet Neurol 2004;3:104–10.

26. Sawcer S, Franklin RJM, Ban M. Multiple sclerosis genetics. Lancet Neurol 2014;13:700–9.
27. International Multiple Sclerosis Genetics Consortium (IMSGC). Analysis of immune-related loci
identifies 48 new susceptibility variants for multiple sclerosis. Nat Genet 2013;45:1353–60.
 2 Pathology

The neuropathological examination of affected brain and spinal cord

tissue has driven MS research for more than 170 years, and in large
part has shaped concepts of pathogenesis, tissue injury and repair.
In contrast to gray matter, which contains neural cell bodies, white
matter predominantly contains myelinated axon tracts. MS is
characterized by the presence of multifocal lesions or ‘plaques’,
predominantly in the white matter, which exhibit myelin destruction,
perivascular inflammation and relative preservation of axons. It is
now recognized that there is considerable gray matter involvement in
MS as well as diffuse white matter pathology that contributes to
long-standing disability.
The condition is traditionally regarded as a T-cell-mediated
inflammatory demyelinating disease, initiated outside the CNS by
loss of tolerance to one, or a number of, CNS antigen(s). This
hypothesis is now regarded as an oversimplification, and
neuropathological, biomarker and treatment studies have implicated
B cells, regulatory T cells and factors within the CNS as critical
pathophysiological determinants.
Lesion distribution
The number, size and distribution of lesions vary widely among
individuals with MS. In early disease, most patients have small
circumscribed lesions that typically occur in the periventricular and
subcortical white matter, corpus callosum, optic nerves, cerebellum
and spinal cord (Figure 2.1). More diffuse white matter pathology
and early gray matter lesions are visualized using recently developed
MRI techniques, as well as in pathological studies. Whole-brain
volume loss, which is now known to commence early in the course
of MS, is likely to be associated with both diffuse and discrete
changes that lead to brain atrophy.
Although disease may be macroscopically confined to the white
matter, careful neuropathological evaluation reveals focal cortical and
deep gray matter lesions in almost all patients with MS (Figure 2.2).
Rarely, patients present with large tumor-like (‘tumefactive’)
hemispheric lesions that can be mistaken for primary brain
neoplasms until typical pathological changes of MS are identified on
biopsy tissue.

Figure 2.1 Whole-brain coronal section from a patient with

secondary progressive MS. Typical small chronic lesions are present
in the corpus callosum (asterisk) and periventricular white matter
(arrow) of both hemispheres. Remyelinated lesions, which stain
palely for myelin, are also present (arrowhead). Small leukocortical
lesions are visible at higher power in both hemispheres. Luxol fast-
blue.

Figure 2.2 The edge of a chronically demyelinated cortical lesion,

which also involves the adjacent white matter, in a patient with
secondary progressive MS. Note the reduction in neuronal density in
the demyelinated (upper) zone of gray matter. Luxol fast-blue cresyl
violet.

Many MS lesions are associated with cerebral vessels, and some

contain a small central vein. Indeed, higher-tesla MRI and newer
imaging techniques have shown that over 80% of MS lesions have a
central vein sign.1 High-field MRI and lesion location are radiological
features that can help to differentiate MS lesions from vascular brain
lesions and as such may help to end the debate as to whether a
central vein is needed to confirm an MS lesion.
Chronic lesions
Well-circumscribed, chronic, hypocellular, white matter plaques
predominate in most patients with longstanding MS. Most of these
lesions are devoid of myelin and exhibit relative axonal preservation
(Figure 2.3). Few mature oligodendrocytes are present, and there is
variable astrocytic proliferation and gliosis. Some chronic lesions may
have a fringe of thin myelin sheaths at the plaque border,
representing remyelination. Conversely, active breakdown of myelin
sheaths may be present at the edge of slowly expanding chronic
plaques (chronic active plaques), a frequent finding in some patients
with secondary progressive MS.2 It has been suggested that these
‘smoldering’ lesions strongly contribute to the worsening of
symptoms in the progressive phase of MS.3
Acute lesions: implications for pathogenesis
The hallmark of the acute MS lesion is the abrupt appearance of
large numbers of activated microglia and macrophages,
outnumbering lymphocytes by at least 10–20 times, in concert with
the start of myelin breakdown and focal disruption of the blood–
brain barrier. Active lesions, which predominate in early relapsing
MS, are defined pathologically by the presence of partially
myelinated axons in tissue infiltrated by macrophages. When stained
with Luxol fast-blue (a stain for myelin), these macrophages are
found to contain myelin particles that are immunoreactive for myelin
proteins (Figure 2.4). Most of the macrophages, which display
enhanced expression of CD45 and MHC class II antigens, appear in
sheets and are thought to derive primarily from resident microglia,
rather than circulating monocytes.

Figure 2.3 A small well-circumscribed lesion in the deep white

matter of a patient with established MS. The lesion is completely
devoid of myelin, has relatively well-preserved axons and exhibits a
moderate degree of astrogliosis. Luxol fast-blue.

Figure 2.4 Classic active lesion in early relapsing MS. Partially

myelinated axons are infiltrated by numerous macrophages
containing particles that immunostain positively for myelin. Myelin-
oligodendrocyte glycoprotein.

The nature of the macrophage ‘attack’ on apparently normal

myelin is unclear. In the most widely accepted paradigm, phagocytic
activity is directed by myelin-specific T cells in perivascular cuffs and,
in lesser numbers, diffusely infiltrating the parenchyma within such
lesions. The process is facilitated by the secretion of injurious toxins,
including tumor necrosis factor (TNF) α, reactive oxygen species and
proteolytic enzymes. This hypothesis has been challenged by the
neuropathological interrogation of ultra-acute (newly forming) MS
lesions, which are characterized by extensive loss of
oligodendrocytes without significant T-cell infiltrates.4 Whatever the
cause, myelin loss from axons proceeds rapidly and is usually
complete within 2 weeks of symptom onset. Lesions examined
during this time show a variable reduction in oligodendrocyte
numbers and evidence of at least modest axonal injury.
Normal conduction in surviving axons is disrupted by the
inflammatory milieu and demyelination, resulting in slowed impulse
conduction. A proportion of demyelinated fibers are unable to
support impulse conduction, in part because of a low density of
sodium channels in the axon membrane, resulting in ‘conduction
block’ and the development of neurological symptoms.
Compensatory alterations in the redistribution of ion channels
(sodium/potassium) underlie responses to drugs such as potassium-
channel blockers (for example, fampridine). Paradoxically, it is
precisely these physiological changes that may contribute to
increased metabolic ‘stress’, which in turn may hasten axonal
damage.
The periplaque white matter
The periplaque white matter is the zone immediately surrounding
acute and chronic MS lesions. It is characterized by the presence of
activated microglia (which may form specific elongated ‘nodules’ or
aggregates; Figure 2.5), perivascular T-cell cuffs and proliferating
oligodendrocytes. While poorly defined, the molecular events that
take place in the periplaque white matter are probably critical to
both lesion formation and repair.

Figure 2.5 Extensive microglial activation in the normally

myelinated periplaque white matter of a patient with secondary
progressive MS. Occasionally, microglia in the periplaque white
matter may form elongated nodules, possibly around short axon
segments that are immunoreactive for complement (C3d). CD68.
Remyelination
Recovery from relapses is in part mediated by remyelination, the
process by which denuded axons are enveloped by new myelin
sheaths (Figures 2.6 and 2.7). New myelin is laid down by a
population of oligodendrocytes that appears within lesions only days
after an episode of acute inflammatory demyelination. These
myelinating cells are derived from oligodendrocyte progenitor cells,
which must migrate from the periplaque white matter and mature
before commencing the process of axon ensheathment.
Although remyelination is the default response to demyelination in
early relapsing disease, the process progressively fails with
advancing disease and age in many patients. The subsequent loss of
myelin-associated trophic signals contributes to axonal degeneration
and the accrual of irreversible disability.5 The molecular mechanisms
that underpin remyelination failure are yet to be fully elucidated, and
current MS therapies, which effectively target inflammatory
pathology in early disease, do not promote endogenous repair
mechanisms or arrest disease progression. Although a Phase II
randomized controlled trial (RCT) of anti-LINGO1, a humanized
monoclonal antibody designed to promote remyelination and restore
function, showed potential enhancement of remyelination following
acute optic neuritis,6 a subsequent randomized dose-ranging Phase
II study of anti-LINGO1 in relapsing MS failed to show any
improvement in disability compared with placebo.7
Figure 2.6 Remyelination begins soon after demyelination is
complete in the early relapsing phase of MS. Thinly (re)myelinated
axons are interspersed by numerous lipid-laden macrophages in this
recently active spinal cord lesion. Oil Red O.
‘Neurodegeneration’ and gray matter lesions
Although myelin appears to be ‘targeted’ in MS lesions, focal and
diffuse axonal loss is present in the white matter of patients with
relapsing and progressive forms of the disease (see pages 29–33).
Diffuse white matter axonal loss becomes most prominent in
longstanding disease, and is accompanied by diffuse activation of
microglia and the presence of scattered perivascular T-cell cuffs.8
This so-called neurodegenerative component of MS correlates
strongly with the development of irreversible disability and MRI
measures such as whole-brain atrophy.

Figure 2.7 Principal pathological features of early/late

remyelination. In early relapsing MS, the process of remyelination
begins soon after a demyelinating event, indicated here by the
presence of Oil Red O-positive macrophages. The circled numbers
represent potential sites for dysregulation of remyelination: NG2+
oligodendrocyte progenitor cells (OPCs) (1) proliferate in periplaque
white matter (PPWM) surrounding recently demyelinated tissue and
(2) migrate into the plaque. Here, they (3) differentiate into
myelinating oligodendrocytes that (4) ensheath denuded axons with
new myelin lamellae. Neuropathological examination at this time
may reveal older Periodic acid–Schiff (PAS)-positive macrophages.
With time, fusion of myelin lamellae promotes (5) the formation of
compact myelin.

While MS is traditionally regarded as a white matter disease,

prominent demyelination, neuroaxonal injury and loss of synapses
are present in the cortex and deep gray matter of patients with
longstanding disease and underpin the cognitive and, to a lesser
extent, motor dysfunction that characterizes this phase of the
condition.
Focal gray matter lesions are less inflammatory than their white
matter counterparts, likely a reflection of reduced myelin density in
the gray matter rather than any fundamental difference in lesion
pathogenesis. Focal cortical lesions are, however, often
topographically related to meningeal lymphoid aggregates,
implicating a local effect of T or B cells.9,10 An analysis of brain
biopsies from patients with early or acute MS suggests that focal
cortical pathology may also be common in early disease.10
Concordant with this finding, neuroimaging studies indicate that
brain volume loss preferentially occurs in the gray matter in early
relapsing MS.11

Key points – pathology

• Early relapsing MS is a multifocal inflammatory
demyelinating and degenerative disease that affects both
the white and gray matter.
• MS leads to a diffuse change in the white matter, which
explains the brain atrophy that occurs early in the disease
course.
• Although still considered to be an organ-specific
autoimmune disease, loss of myelin-forming
oligodendrocytes in newly forming MS lesions is a critical
event that may trigger or amplify the inflammatory
cascade that characterizes active demyelination.
• Resolution of inflammation, restoration of axonal impulse
propagation and remyelination mediate recovery from
discrete clinical relapses in early disease.
• Molecular reorganization of demyelinated axon
membranes, characterized by a greater than normal
sodium-channel density, permits the restoration of
continuous impulse propagation in non-remyelinated
fibers.
• As the disease advances, the pathological complexity of
MS increases. Multifocal adaptive inflammation is
progressively replaced by a diffuse ‘degenerative’ phase,
although these two facets of MS neuropathology are
probably inextricably linked.
• Current therapies effectively target the inflammatory
pathology that peaks in early disease. It is hoped that
future therapies will be able to arrest the progression of
established ‘neurodegeneration’ and/or promote
endogenous repair mechanisms such as remyelination.

Key references
1. Kilsdonk ID, Wattjes MP, Lopez-Soriano A et al. Improved differentiation
between MS and vascular brain lesions using FLAIR* at 7 Tesla. Eur Radiol
2014;24:841–9.
2. Prineas JW, Kwon EE, Cho ES et al. Immunopathology of secondary-
progressive multiple sclerosis. Ann Neurol 2001;50:646–57.
3. Frischer JM, Weigand SD, Guo Y et al. Clinical and pathological insights
into the dynamic nature of the white matter multiple sclerosis plaque. Ann
Neurol 2015;78:710–21.
4. Barnett MH, Prineas JW. Relapsing and remitting multiple sclerosis:
pathology of the newly forming lesion. Ann Neurol 2004;55:458–68.
5. Fancy SP, Kotter MR, Harrington EP et al. Overcoming remyelination
failure in multiple sclerosis and other myelin disorders. Exp Neurol
2010;225:18–23.
6. Cadavid D, Balcer L, Galetta S et al. Evidence of remyelination with the
anti-LINGO-1 monoclonal antibody BIIB033 after acute optic neuritis.
American Academy of Neurology Annual Meeting 2015, Chicago, IL, USA,
Scientific program, poster 008.
7. Cadavid D, Mellion M, Hupperts R et al. Safety and efficacy of opicinumab
in patients with relapsing multiple sclerosis (SYNERGY): a randomised,
placebo-controlled, phase 2 trial. Lancet Neurol 2019;18:845–56.
8. Kutzelnigg A, Lucchinetti CF, Stadelmann C et al. Cortical demyelination
and diffuse white matter injury in multiple sclerosis. Brain 2005;128:2705–
12.
9. Howell OW, Reeves CA, Nicholas R et al. Meningeal inflammation is
widespread and linked to cortical pathology in multiple sclerosis. Brain
2011;134:2755–71.

10. Lucchinetti CF, Popescu BF, Bunyan RF et al. Inflammatory cortical

demyelination in early multiple sclerosis. N Engl J Med 2011;365:2188–97.
11. De Stefano N, Matthews PM, Filippi M et al. Evidence of early cortical
atrophy in MS: relevance to white matter changes and disability. Neurology
2003;60:1157–62.
3 The clinical picture
A brief history
Historically, the earliest personal account of MS was recorded in the
diaries of Frederick D’Este, grandson of King George III. Although
his condition was not diagnosed in his lifetime, from 1822 to 1846 he
kept a detailed log of his symptoms, which included transient loss of
vision, clumsiness of the hands, weakness of the legs, incontinence
and dizziness. MS became recognized as a clinicopathological entity
around 1870, when Charcot noted a link between the symptoms of
MS and nerve damage. Over the next 50 years, various hypotheses
were promulgated, including an infectious cause, and oligoclonal
bands were discovered in the cerebrospinal fluid (CSF). By 1950, it
was clear that MS was a disease of the CNS and by 1960, the
beneficial effect of steroids in the management of acute relapses had
been identified. By the 1990s, the first injectable disease-modifying
therapies (DMTs) were in use. In 2001, the McDonald criteria for the
diagnosis of MS were revolutionized by the incorporation of MRI to
demonstrate dissemination of lesions in space and time.1
We now know that MS is an inflammatory, demyelinating and
neurodegenerative disease that affects multiple sites across the CNS.
The clinical phenotype of MS depends largely on the location of
inflammatory lesions, resulting in a broad spectrum of symptoms
and signs. While the majority of individual lesions, particularly within
the cerebral hemispheres, are asymptomatic, pathology in ‘eloquent’
areas such as the optic nerve, spinal cord and brainstem is usually
accompanied by a relevant clinical syndrome.
Definitions
Clinically isolated syndrome. The term ‘clinically isolated
syndrome’ (CIS) has previously been used to describe the first
presentation of demyelination. However, following revisions to the
McDonald criteria in 2010, a diagnosis of MS can now be made
following the very first attack if the initial MRI shows evidence of
dissemination in time (both enhancing and non-enhancing lesions)
and space.2 The term ‘clinically isolated syndrome’ is no longer in
favor as it suggests diagnostic uncertainty for the patient and the
physician.

Multiple sclerosis. A person has clinically definite MS when there is

objective clinical evidence of lesion dissemination in time (DIT) and
space (DIS). The second clinical episode must occur in a different
site from the original lesion at least 1 month later. When reviewing a
patient with CIS or MS, a detailed neurological history and
examination must be taken to search for evidence of new symptoms
or signs of CNS demyelination. Importantly, the incorporation of MRI
and CSF features into modern diagnostic criteria permits a diagnosis
of MS to be made in some patients at the time of the CIS.

Radiologically isolated syndrome. Increasing use of MRI to

investigate neurological symptoms has resulted in an increase in
incidental findings. A person has a radiologically isolated syndrome
(RIS) if MRI is suggestive of MS but they have had no clinical
episodes and the neurological examination is normal. In one study of
people with RIS, one-third had developed a clinical episode at 5
years.3
Types of multiple sclerosis
It is important to define the subtype (or phenotype) of MS, as this
can guide prognosis and choice of DMT. For example, therapies that
reduce the frequency and severity of relapses may not be helpful to
people with progressive disease. As all the available treatments have
potential side effects, all patients should be provided with a risk–
benefit analysis appropriate to their MS subtype. The traditionally
recognized patterns of MS are:
• relapsing remitting (RRMS)
• secondary progressive (SPMS)
• primary progressive (PPMS)
• progressive relapsing (PRMS).

Figure 3.1 The two patterns of RRMS: (a) relapses with return to
normal neurological function; (b) relapsing disease with stepwise,
accumulated disability.

Relapsing remitting disease is the most common form of MS,

accounting for 65–70% of patients. RRMS is characterized by periods
of acute neurological disturbance (relapses), which last for at least
24 hours and are not attributable to other causes such as infection
or changes in core temperature. These relapses must occur after
more than 30 days of clinical stability, and the neurological deficit
must be established objectively by clinical evaluation (history and/or
examination).
In early disease, recovery after a relapse (remission) is often near
complete, but incomplete recovery is common in established disease
with patients often accruing disability with each successive relapse
(Figure 3.1).

Secondary progressive disease. In most cases (up to 75% of

people with RRMS), there is an eventual progression to SPMS. This is
defined as an initial relapsing remitting disease course followed by
progression with or without occasional relapses, minor remissions
and plateaus (Figure 3.2). Risk factors for progression to SPMS are
shown in Table 3.1. 4 The progression of disease from relapsing
remitting to the secondary progressive stage is usually noted
retrospectively: for example, when a patient with MS has
accumulated disability over 6–12 months without any discrete
episodes of relapse. Neuroaxonal loss without any ‘overt’ features of
inflammation (clinical or radiological) is thought to underlie this
phase of MS (Figure 3.3).
Figure 3.2 In SPMS, patients (a) may or (b) may not continue to
have relapses.

TABLE 3.1

Risk factors associated with progression to SPMS4

• Older age at disease onset
• Short interval between the first and second relapses
• Higher and increasing T2 lesion load
• Motor deficit with incomplete recovery

Primary progressive disease comprises approximately 10–15% of

patients with MS. It does not present with discrete relapses, but a
gradual progression of disability, often attributable to spinal motor
involvement (Figure 3.4). PPMS typically has a later onset than
RRMS.
Figure 3.3 The natural history of MS. Silent inflammatory activity
almost certainly begins before the first clinical event (CIS). Lesions
compatible with inflammatory demyelination discovered incidentally
by MRI during the preclinical phase represent the RIS. The
incorporation of MRI into modern diagnostic criteria permits
determination of DIT in the absence of a second clinical event, when
new T2 (or contrast-enhancing) lesions are present on follow-up
imaging. The 2010 McDonald criteria first permitted a diagnosis of
MS to be made at the time of a CIS if there are both enhancing and
non-enhancing lesions (indicating DIT) on MRI. In parallel with the
development of relapses and new T2 lesions, there is progressive
loss of axons, neurons and synapses from the earliest phases of the
disease, which manifests clinically with secondary progression when
neuroaxonal reserves are exhausted, indicated here by the ‘clinical
threshold’. In this secondary progressive phase of MS, acute discrete
inflammatory events (contrast-enhancing lesions, new T2 lesions)
wane and progressive brain atrophy dominates the MRI picture.

Progressive relapsing disease. A small number of patients

present with gradually progressive disease onto which are
‘superimposed’ periods of worsening that may be steroid responsive
(Figure 3.5). While a clear history of discrete relapsing remitting
symptoms may be lacking in these patients, a proportion may have
acute (gadolinium-enhancing) MRI lesions and respond to
immunomodulatory therapies. Progressive relapsing disease should
therefore be differentiated from primary and secondary progressive
disease.
Figure 3.4 Typical pattern of progressive disability in PPMS.

Figure 3.5 Pattern of disease in PRMS – progression of disability

with ‘superimposed’ periods of worsening.

Updates to definitions. In 2013, the International Advisory

Committee on Clinical Trials of MS re-examined the above definitions
of MS phenotypes,5 which were previously outlined in 1996.6 It
recommended that ‘active’ disease in both the relapsing and
progressive forms of MS should be defined by the presence of
clinical relapses or new/enhancing MRI lesions. It also recommended
that the presence or absence of progression over a given time period
should be determined as part of the description of both the primary
and secondary progressive subtypes. These modified descriptors
should enhance the characterization of MS and have utility in both
clinical and research settings.
Patient history
Medical history. People with MS do not always seek medical
attention in the early phase of the disease, especially when the
sensory pathways are affected in isolation or if symptoms such as
visual blurring are mild and temporary. However, it is important at
presentation to determine whether a patient presenting with an
apparent CIS has experienced a prior remitting neurological
disturbance of any sort (Table 3.2).
L’hermitte’s sign is an unpleasant paroxysmal sensation, often
described as an electrical shock radiating along the spine and into
the limbs, which is usually provoked by neck flexion. This indicates
that there is an ‘irritative’ lesion at the level of the cervical cord and
is thought to be due to stretching of hyperexcitable neurons in the
dorsal column. It is common in MS but can be associated with other
causes of cervical spinal cord disease, such as cord compression,
vitamin B12 deficiency and radiation myelopathy.
Uhthoff’s phenomenon is the worsening of neurological
symptoms as core body temperature increases: for example,
increased visual blurring after a hot shower or worsening of pre-
existing limb weakness in high ambient temperatures.

TABLE 3.2
Useful questions for ascertaining prior neurological
disturbances

Have you ever experienced numbness or heaviness in any of your

limbs, particularly in association with changes in bladder or bowel
function, that went away before you sought medical help?
Have you ever experienced numbness or a feeling of a tight band
across or around your trunk?
 Have you ever had a painful eye or a loss of vision that lasted for
a few days or weeks?
Has your color vision ever been affected?
Have you ever had double vision that lasted for more than a day?
Have you ever had vertigo or balance difficulties (ataxia) that
lasted for more than a few days?

Other autoimmune diseases. As there is an association

between MS and other autoimmune diseases, such as thyroid
disease, diabetes mellitus, vitiligo and inflammatory bowel disease, it
is important to include questions about these when taking a history.

Family history. The risk of MS rises with increasing genetic

proximity to an affected individual (see Table 1.1, page 14). It is
therefore important to document any family history of MS or
autoimmune diseases (which are often familial). The onset of MS
tends to be earlier in people with familial MS.

Social history. Smoking is a risk factor for MS. It is also important

to establish country of origin and time of migration when trying to
establish the likelihood of MS (see Chapter 1).
Signs and symptoms
MS manifests with symptoms or signs that arise from focal
inflammatory lesions within the CNS. These can be localized by
taking a thorough history and by clinical examination. The symptoms
associated with an MS relapse usually evolve over 24 to 48 hours,
and persist for at least 24 hours, often improving gradually over
subsequent days and weeks. Although ‘eloquent’ regions of the CNS,
such as the spinal cord, optic nerve and brainstem, are more likely to
result in symptoms (Table 3.3), the spectrum of presenting
symptoms associated with demyelination is broad. These may
include any cranial nerve palsy, facial myokymia, trigeminal or
glossopharyngeal neuralgia, specific spinal syndromes such as
deafferented limb and Brown–Sequard syndrome, and seizures.
However, only a minority of new lesions (approximately 1 in 10) in
the hemispheric deep white matter are symptomatic.
Relapse risk may be heightened by recent urinary or respiratory
tract infections, or other bacterial or viral infections, which should be
documented. Relapses must be differentiated from physiological
‘pseudorelapses’ that may occur in the context of infection-related
fever. A history of recent vaccination may also be relevant, although
prospective studies have not identified a relationship between
common vaccines, such as influenza and hepatitis B, and MS
relapse.7

TABLE 3.3
MS symptoms at presentation and during the course of
the disease8

Symptom Presenting (%) During course (%)

Visual/oculomotor 49 100
Another random document with
no related content on Scribd:
cheerfully took his turn at the pump, and so saved the captain and
me any anxiety on that account.
It had been no pleasure cruise after we passed Brisbane, and
became worse every day. There was not a dry place on board,
unless it was our throats. Everybody was constantly drenched with
the sea, and no one had a good square meal during the last four
days; but there was no discontent, everything was taken in good
part, and many a tough yarn was told while they were lashed to the
rail to keep themselves from being washed overboard.
After two days sheer battling for our lives, the wind died down, and
a steady southerly wind sprang up. This soon brightened our
prospects, and added considerably to our comfort. How thankful we
were for the peace and quiet after the rough and tumble experience
we had just passed through! The sea became as smooth as a mill
pond with just a steady south wind blowing, that drove us about five
knots an hour through the water. All our effects were brought on deck
and dried, and our sails, which had been considerably damaged,
were repaired, and on the fourteenth day we arrived at Cookstown.
Our passengers were soon landed, and Captain Brown took the little
vessel well into the river and moored her there until he decided what
he was going to do himself. I landed the following day, and soon
found that the Palmer was as far off as ever. The rainy season had
set in, and the roads were impassable. Whole districts between
Cookstown and the Palmer were under water, the rivers were
swollen and in flood, and no stores of any sort could be bought on
the road.
To describe Cookstown as I first saw it would be impossible. It
resembled nothing so much as an old English country fair, leaving
out the monkeys and merry-go-rounds. Tents were stuck up at all
points. Miserable huts, zinc sheds, and any blessed thing that would
shelter from the sun’s fierce heat and rain, were used as habitations.
There were thousands of people living in the tents and sheds, and
the place literally swarmed with men of all nationalities. Large plots
had been pegged out in the main street, on these were erected
either corrugated iron sheds, or large tents, and here all sorts of
merchandise was sold, cheap enough to suit all purses, but the wet
season was on, and there was no way of getting to Palmer. Parties
of men left every day in the rain and slush to try and reach what
seemed such a land of promise, but many returned saying that it was
no use trying, as the rivers could not be crossed. Hundreds of these
men lived out in the scrub with just a couple of blankets thrown over
some twigs for shelter, no fire being needed except for cooking. All
the scum of Melbourne, Sydney and Brisbane were gathered
together here, thieves, pickpockets, cardsharpers and loafers of
every description. This class had not come to dig for gold with pick
and shovel from mother earth’s bosom, but to dig it out of honest
men’s pockets by robbery and murder, and the robbing of tents in
their owners’ absence was becoming a daily occurrence, for
gathered there were the good, bad, very bad and indifferent.
One day a party of three men returned after having got as far as
the Normanby River. They had been caught between two streams,
and could neither get backward or forward. The patch on which they
were imprisoned was only a few feet above water, and for some time
they were not sure if they would not be swept off and drowned, as
the island was only about one mile long and a quarter of a mile wide.
Whilst they were searching for means to get over to Normanby
they made a gruesome discovery, one by no means uncommon.
There at their feet lying together were five dead bodies. They had
been starved to death, and under the head of each man was a small
leather bag of gold, averaging in weight about six pounds each.
What a terrible irony of fate—shut in between the waters and starved
to death, with over five thousand pounds between them! The bodies
were all shrunken and black, so burying them where they lay, the
party took the gold and divided it. A couple of days afterwards they
were able to swim their horses over the stream and return to
Cookstown.
There were several instances told about this time of miners who
had reached the diggings before the wet season had set in, gathered
a stock of gold, then finding their stores giving out, were forced to
pack up and retrace their steps for a fresh supply. Many, on that
terrible return journey, were struck down by the sun’s intense heat,
and after using their last small stock of food, died a miserable lonely
death by starvation, their treasures of gold powerless to buy them an
ounce of food.
 It was quite a common occurrence for miners travelling up from
Cooktown with plenty of stores and provisions, but no cash, to arrive
on the banks of a swollen river, over which there was no means of
crossing, and to see on the other side of the river a party of men on
their way down to the coast with bags of gold, but with hungry, empty
stomachs. There they were, looking across at each other, one
holding up a bag of flour, and the other shaking his gold purse, each
powerless to help the other. Such was the lot of many of the diggers
at that time, but all the horrors, the suffering and death that took
place in that mad rush for gold, will never be known. ’Tis better so, I
saw men return from the gold fields, with thousands of pounds worth
of gold in their possession, but with frames so emaciated and ruined
with what they had gone through on their return journey, that their
very existence was a burden to them, their horses, dogs, and even
their boots had been eaten to keep them alive. It is a fact that they
have boiled their blucher boots for a whole day, and then added any
weeds they could find to make a broth of, so tenacious of life were
they.
There were hundreds of men idle in Cooktown. They had no
means of buying an outfit, even if the road to Palmer had been
passable, and many of them had no desire to go any further. These
could easily be distinguished from those who really wanted work
during the waiting time, so many there were that anyone who wanted
a man might easily get him for a whole day’s work for a good square
meal. Men would walk about among the tents and whenever they
saw food there they would beg. Many were getting a living by their
wits and knavery, and it was not safe to be about alone after dark,
unless you were well armed and prepared for these light-fingered
gentry. And yet the leading articles in the newspapers at that time
were painting in glowing terms the bustle and activity going on in the
rising city of Cooktown, declaring that any man who could use a
hammer or tools of any description could earn a pound a day.
Feeling a bit disheartened at the grim realities that I had
witnessed, and after knocking about Cooktown for a week, I called
on Captain Brown, and asked him if he was going to take the
“Woolara” back to Newcastle.
 “No,” he replied, “I have sold her, and made a jolly good thing out
of her, too, and I’m going to have a try to get to the Palmer. What are
you going to do?”
“Well, I am undecided at present, there are so many returning
disheartened, and broken down in health, and they give such bad
accounts of the road to be travelled over before you reach the
Palmer, that I don’t care about tackling it alone.”
“Well, look here,” said the captain, “I have done very well by this
venture so far, and I don’t care about returning without having a try
for the diggings, even if I have to return. What do you say to us
joining forces, and trying our luck together. I will buy three horses
from the next squad that returns, and use one for a pack horse.”
I agreed to his plan, and the following day about a dozen
horsemen rode into Cooktown. They had been a month on the road,
several times they had narrowly escaped drowning, while trying to
cross the Normanby river. They had lost nearly the whole of their
provisions, and one of their mates had been seized by an alligator
before their eyes, while they were powerless to help him. Then they
had been obliged to kill two of their horses for food. They willingly
sold us three horses at fifteen pounds each, but strongly advised us
not to try the road for at least two months, or to wait for the end of
the rainy season. But the thought of the gold beyond made us eager
to take our chance. Had we gone back to Newcastle without trying,
our friends would have chaffed us unmercifully.
The next day we began our preparations. We bought a tent, two
small picks, two small spades and one gun. Captain Brown had a
gun and revolver. I had a revolver, and the gun that was bought was
for me, and a good supply of ammunition. As we were going where
money was of no value and food invaluable, and everything
depended on our being able to carry sufficient provisions, we got a
good supply of the best. We had cocoa, extract of beef, preserved
meat, tea and sugar, two hundred pounds of flour—this was divided,
one hundred pounds to the pack horse, and fifty pounds to each of
our horses—two large billy cans, a couple of drinking pots, two
knives, two basins, a tinder box and burning glass. When we were all
packed and ready to start, we looked like a couple of mountebanks
off to a village fair.
 It was a fine morning when we started, but before we had got ten
miles from Cooktown our horses were sinking in the mire. Road
there was none, it was just a track or belt of morass, into which one
sank at times knee deep, and as night came on it rained in torrents,
so we picked out a dry piece of ground, and pitched our tent for the
night. We then hobbled the horses with about ten fathoms of line to
keep them from straying.
We slept well that night, for we were dead tired, and had we been
lying on a feather bed in a good hotel instead of on a piece of ground
that might soon be under water, we should have slept no better. As it
had ceased raining when we awoke we started on our way again
after we had breakfasted, and got along very well until noon. Coming
to a place where there was good grass for the horses we decided not
to go any farther that day, but to let the horses have the benefit of a
good feed.
The following morning we started early, and at noon met a party of
diggers returning from the Palmer. They had been fortunate enough
to get a fair amount of gold they said, but what a terrible condition
they were in, thin and emaciated as skeletons, with barely a rag to
cover them. Three of their party had been lost crossing the Laura
river, and one had died of sunstroke on the road.
“What is it like further ahead, mates?” asked Brown.
“Well, it is only just passable to the Normanby river from here. I
don’t think you will be able to cross it with your packs. We had to
swim it, holding on to the horse’s tails, and then we lost some of our
little stock of food, it was a narrow squeak for us all, horses and men,
but we are here, thank God, safe so far.”
Brown gave them a small tin of beef essence, and a few ship’s
biscuits that he had brought with him. The gratitude of the poor
hungry fellows was pitiful to see, then they offered us some of their
hardly won gold for it, which we promptly refused.
“No, no, mates,” said Brown. “You chaps have earned and suffered
enough for that. Keep it, and take care of it, and may you live to
enjoy it.”
We camped all together that night, after sitting yarning for some
hours, and when we had all eaten a very hearty breakfast we
separated, each party going on its way, like ships that pass in the
night, never to meet again.
Our track that day was very bad, just slush and mire, the horses at
every step sinking up to their knees. We were ready and expected to
meet with hardship on the road, but to realize the suffering to man
and horse dragging themselves along that quagmire is better felt
than described. Every moment we were afraid of them breaking
down, and when about two p.m. we got on a stretch of solid ground,
we pitched our tent, and gave them a good rest. So far we had not
seen a living bird or animal since leaving Cooktown. Had we been
depending on our guns supplying our larder with food we should
have had to go short, fortunately for us we were not.
The next day it was terribly hot, and, to add to our discomfort, we
had several heavy showers, which soon wet us through and through.
When these stopped and the sun came out again our clothes
steamed on us, just as though we were near a fire; this and the
steam arising from the ground made us feel faint and feverish. We
were also pestered with a common little house fly that swarmed
around us and was a perfect nuisance. At sunset we felt we could go
no farther, so pitched our tent on a patch of stony ground close to a
creek, where there was good grass, so we hobbled the horses and
let them graze.
We turned in early, for we were dead tired, and the mosquitoes
were buzzing round in myriads, with their incessant cry of “cousin,
cousin,” when about midnight we were roused by a tremendous row
near us, a peculiar indescribable noise was coming down from the
creek, which we could not account for. We both sprang up and
seized our guns, but the night was pitch dark. What it might be we
did not know, we did not go out, but remained in our tent on the
defensive. Never had either of us heard anything like it; it was as one
often hears, “sufficient to raise the dead.” We began to wonder if we
were surrounded by a mob of the blacks, who were lurking around
us, or was it the spirits of those who had perished on this lone track,
and who were trying to make us return to civilization, but whatever it
was, it was awful and above all the noise could be heard quite
distinctly—a piercing yell of pain, such as no human being or animal
we knew could utter. Thinking to frighten the blacks, if it were indeed
they, we shouted out to each other in different tones and names, to
give them the impression that we were neither alone or unarmed.
When the welcome daylight came we Went in search of the
horses. We could only find two, but on the bank of the creek, not far
from the tent, was the forepart of our third horse. It was bitten off
right under the forelegs, all the rest was gone. There on the ground
and in the soft mud were the signs of a struggle, and the marks of
some big body having been dragged towards the water. Close to the
water were the tracks of a huge alligator, and where it had come out
of and entered the creek, a deep furrow had been turned up by its
tail. This explained the noise in the night, it was the struggle and
death agony of the poor beast, it must have been drinking at the
creek and been seized by the alligator. This was a very serious loss
to us, and made us feel quite disheartened.
We remained where we were until noon. Then crossed the creek
and went on our way—our horses more heavily weighted than before
owing to the loss of the packhorse—and at sundown we pitched our
tent. Our fire was barely lighted to boil the billy for tea, when three
men crawled up to the tent. We were so surprised, that for the
moment we stood still looking at them, for they looked like
scarecrows with their clothes hanging in rags upon them.
“For God’s sake mates, give us something to eat, we are starving,
we have lost everything crossing the Normanby.”
“Aye, aye, lads,” said Brown. “Come up to the fire, and you shall
share our meal. Have you come from the Palmer?”
“No, we could not get there. It is six weeks since we left Cooktown,
and we are trying to get back. Our provisions gave out, and we could
neither go forward or get back, owing to the district being flooded
and impassable. Three days ago the strength of the river eased
down a bit, and we managed to cross by strapping our bits of
clothes, and the little food we had on the horses’ backs, then we got
on their backs and forced them into the water, but the current was so
great that they were borne down the stream, so we slipped off, and
getting hold of the horses’ tails with one hand, we swam with the
other. We managed to cross, but it was a desperate undertaking, and
we were so done up that we were too weak to tie up the horses. We
just lay where we landed and went to sleep. We never saw the
horses again, and have not the slightest idea what has become of
them. And now mates, we are stranded here, without a bite of food,
and unless you can help us here we must die; we can go no farther.
What is it to be?”
“Well, strangers,” said Brown, “my mate here and I were bound for
the Palmer. We have had a tough job of it so far, and we have had
quite enough of it. Hal a good meal, and rest yourselves well, and
we’ll all go back together.”
The poor fellows could hardly find words to thank him. They ate a
hearty meal, and washed it down with a good pot of tea, and very
soon after were in a sound sleep.
Brown and I sat talking far into the night. To tell the truth I was not
sorry he had decided to return, for with one thing and another, I had
begun to ask myself whether the game was worth the candle, and
seemed all at once to have sickened of the roaming about, and felt
that the ups and downs of sea life were luxury in comparison to
hunting for goldfields.
The following day we divided the stores between the two horses,
and prepared to tramp back to Cooktown.
 CHAPTER XXV

We Return to Cooktown

The first day of our return journey we travelled as far as the creek
where we had lost our horse the day before. The poor fellows we
had rescued were completely done up, so Captain Brown
determined to go along slowly, and so give them a chance to pick up
their strength. Their names, they told us, were James Whitefield,
Henry Bagly and Thomas Pain. Whitefield, it seems, had been on
almost every goldfield in the colonies, and had three times been in
possession of twenty thousand pounds worth of gold. According to
his own account, which I afterwards verified, the man had not a
friend in the world, or a relative living. He was utterly indifferent to
worldly possessions, and after returning from the Victorian goldfields
had spent, or squandered, twelve thousand pounds in Melbourne in
three weeks. A woman in Burk Street took his fancy, and he bought
and furnished a house for her that cost him five thousand pounds,
then, after living with her there for ten days, he grew restless and
cleared out to the Charter Tower goldfields. He could neither read
nor write distinctly, because, as he said, he had no use for either.
The other two men were runaway sailors, who had been working
ashore for twelve months at Brisbane before starting for the Palmer.
The following morning we swam the creek after firing our guns and
shouting to scare any alligators that might be about. The creek was
about two hundred feet across, and for about sixty feet from the
south shore the depth was only about four feet, then the bed
suddenly dropped and the current rushed very strongly until the north
shore was reached, and there the landing was very bad as the scrub
came right down to the water. The way we crossed was as follows: A
small line was made fast to the after part of the saddles and
stretched along each horse’s back and a half hitch round its tail. The
horses were then driven into the water, and at once began to swim
across. Captain Brown and Whitefield hung on to the rope of one
horse, and the other two men and I took the other. Before we started
Brown told me to keep next the horse and watch it closely, and to
keep my sheath-knife handy for fear the current might sweep it away.
Brown’s horse led, and we stood to watch it land. When about half
way across Whitefield let go the rope, and with a swift stroke brought
himself alongside the horse on the lower side, then he kept one hand
on the saddle and used the other to propel himself. This eased the
horse somewhat, and he got over fairly easily.
After they had safely landed, Brown called out to me to ease all
weight off the horse. We started, and I swam alongside the horse like
Whitefield had done. The other men held on to the rope with one
hand and swam with the other, and we got along first class until
about fifty feet from the other side, when I felt my feet touch
something, and my heart came into my mouth. The next minute the
horse seemed to be jerked backward, and terrified he began to
plunge, snorting and neighing. Then I heard Whitefield sing out:
“Cut the rope! Cut the rope!”
I drew my knife, and while holding on to the saddle with my left
hand, reached over and cut the rope near the saddle, in my haste
cutting a gash in the horse’s back. At the touch of the knife, and with
the strain from behind relieved, the horse plunged ahead, and in a
minute we landed. I looked round for the other men, but they had
gone under.
“Whatever was the matter, Brown?” I asked.
“Well I don’t know,” he replied. “We saw the fellows go under, and
saw the horse floundering, and Whitefield called out cut the rope,
and if it had not been cut at that moment, the horse would have gone
under, and you, too, I expect.”
“But what do you think took them under?” I persisted. “We were
going along all right at first. Do you think it was an alligator,
Whitefield?”
“Oh, no,” he replied, “if it had been he would have gone for the
horse first. I think there must be a dead tree, or a snag down there,
and they must have struck it and been drawn down in the eddy. They
are dead enough by this time, anyhow.”
“But good heavens, mates, it’s awful,” said Brown, “to think we all
had breakfast together, and now two of us are dead. Were they
friends of yours, Whitefield, you seem to take it pretty coolly if they
were?”
“No,” he replied, “I didn’t know them. We met on the road over the
Normanby river, and beyond their names, I know nothing about
them, except that they had been sailors. They were jolly good mates
—I know that much, anyhow. As to my taking it coolly, well, mates,
my fussing about it would not bring them back, it may be our turn
next, we are not in Cooktown yet. I expect they suffered less in that
last lap of their race in life, than in any other part, and by this time
they’ll have learnt the grand secret.”
“Well, look here,” said Brown, “spread the tent and make some
tea, and I’ll go along the bank and see if there is any sign of their
bodies washing up.”
Whitefield and I soon had the tent spread, and the tea made. The
horses were hobbled, their loads taken off, and they were turned out
to graze. There was not much grass in the place, but a small shrub
that grew in abundance they ate freely of and seemed to enjoy.
Strange to say, although all our stores had been in the water there
was not much damaged. The two small bags of flour I thought would
have been ruined, but they were not. The water had only formed the
flour into a cake on the outside, but the inside was all right.
When the billy was set on to boil I strolled along the bank to meet
Brown, whom I saw was coming back. When I was close to him I
suddenly espied, about twenty yards from the edge of the river, a
bundle tied up with a stick through it, as though it had been carried
over a man’s shoulder. I walked towards it, and Brown, seeing it too,
walked over towards it. He gave it a kick with his foot, and the next
minute was on his knees untying it.
“Some Johnny’s swag,” he said, as he opened the bundle.
The covering was a piece of tent duck, inside it were a pair of
socks, and a wool shirt, both filthy dirty, rolled up inside the shirt was
a piece of canvas, which had apparently been the sleeve of a canvas
jacket. Both ends were tied with a strong grass like flax, and inside
was about eleven pounds of fine gold, that looked just like birdseed.
“Halves, Brown,” I said.
“Oh, no, not halves, mate,” he replied.
I drew my revolver and covered him.
“Why not?” I asked, my temper rising to a white heat at the sight of
the gold.
Brown smiled:
“Put back that revolver,” he said, “you mad-brained young beggar.
What about the other chap shan’t we give him a bit, he needs it just
as much as we do.”
“Oh, yes,” I replied, feeling a bit ashamed, “I agree to that.”
So we shared it out, five pounds each for Brown and me and one
pound for Whitefield. He thanked us, and said he had no claim to any
share, as he was only a stranger, and we were old mates. Who he
was, or what had become of the owner of the swag will never be
known. It was evident he had come from the diggings and had safely
crossed the river. Perhaps he was another of those without food,
who became exhausted, went mad, under the broiling sun, and had
wandered off, or he may only have lain down to sleep and during the
night had been seized by one of the alligators, which were very
numerous in the Normanby at the early stages of the gold rush. The
truth will never be known.
After we had eaten a good feed of damper and tea, we caught the
horses, loaded them up and continued our journey. It was terribly
rough the first few miles. The track was just a spongy quagmire, into
which we and the horses sank knee deep and could hardly pull our
feet out again so great was the suction. And every now and then the
poor beasts would look pitifully at us, as they bravely tried to get
along. However, just at sunset, we found a pitch of dry ground and
rested there for the night.
The following day we got along a little better, but our stores were
getting very low, and the sky began to look very threatening, and the
next morning we were up and off at daylight, but we had only gone a
few miles when the storm burst over us, and the rain came down in
sheets. We spread the tent, but it leaked like a sieve, while the
thunder and lightning was awful. We were soon wet through to the
skin, and everything else we had was in the same condition. We
were afraid to let the horses stray for fear of losing them altogether.
All night the rain came down in torrents, and when daylight came the
whole face of the country was a sheet of water;
“Pack up, lads,” said Whitefield, “we must get away from here
before the floods come down, and then we shall get bogged and that
will be the end of us. I’ve been through that once, and had to shoot
as good a horse as a man need wish for, he was slowly sinking in the
bog. I could not get him out, and the pitiful look in his eyes as he
sank deeper and deeper was more than I could stand, so I just
ended his misery by putting a bullet in his brain, so let’s get on while
we can.”
We managed to make a pot of tea, for we had very little else by
now, and started off again, but what a journey! Every hole and hollow
was full of water, and first one animal and then the other would
stumble into them, both man and beast, I think, had the roughest
time of their life that day, for at the best of it we were nearly up to our
knees, and sometimes a good bit above them. At sundown Brown
wanted to camp, but Whitefield urged us to push ahead until we
reached more solid ground. After a few miles of this quagmire, which
seemed to get worse, and when it was near midnight, we came up to
some bushes or scrub; we found the ground was a little higher and,
though still wet and sloppy, we felt we could go no further, so here
we camped for a few hours’ rest.
At daylight we found, to our surprise, that we were near a camp of
men making for the Palmer. There were quite twenty of them, and
they seemed to be well supplied with stores and horses, in fact, they
looked the most likely and best equipped party that I ever saw on the
way to the goldfields. They had two light-built carts, made specially
for that purpose. These carts were four-wheeled, of light, tough
material, the seams were well puttied and painted and over all the
outside was a cover of strong painted canvas, with two cane wood
runners underneath. When crossing the rivers, the horses were
taken out of the shafts, and the harness was put into the cart with the
stores, the horses would then swim over to the other side, taking the
end of a long line with them. On landing, the other end of the line
was made fast to the cart, and the horses who were on the river
bank easily pulled it across, thus keeping the stores dry. It was a
capital idea and had been well thought out, and would answer its
purpose well. They also had with them a powerful dog of the
Newfoundland breed that had been trained to swim across the
creeks and rivers with a light rope. The party were prepared for any
emergency that might offer itself, and their outfit must have cost a
good sum of money. When Whitefield saw them he offered to go and
assist them for his food, until they arrived at the diggings. Such was
the fascination that the goldfields held for this man. The party readily
accepted the offer of his services, and he joined them at once.
After watching the party start off, we also continued our journey,
and arrived in Cooktown twenty-four hours later. Many were the
enquiries made of us as to the state of the roads and prospects of
reaching the Palmer. There were still hundreds of men waiting in
idleness at Cooktown for the rainy season to pass. The place
seemed worse than when we left it, for wherever you turned there
were the loafers hanging round in scores. Brown was able to dispose
of his horses and tent for forty pounds, clearing ten pounds by the
deal, for horses were scarce and dear, and he might have got more if
he had stood out for it. We sold our gold to the bank and received
from them cash and notes to the value of two hundred and ten
pounds each. Then we put up at a second class restaurant and that
day I posted a money order, value one hundred and fifty pounds, to a
friend in Sydney, to bank for me until I came back, and in the event
of my death it was to be sent to my mother in Liverpool, and Captain
Brown posted a draft to his wife at Newcastle, New South Wales. It
was not safe by any means to have it known about the town that you
had any money on you, especially after dark, as there were plenty of
men in Cooktown at that time who would have cut your throat for
half-a-crown, and think themselves well off to get that much.
 CHAPTER XXVI

A Trip to the Cannibal Islands and Captain

Brown’s Story

We stayed together in Cooktown for a couple of weeks, and then

Captain Brown was offered the command of a small vessel trading
between Cooktown, Townsville, and the Solomon Islands, sometimes
calling at Port Moresby, New Guinea. He at once offered me the
berth of mate in her, and I gladly accepted, as it was quite a new part
of the world to me, and just what I wanted. The “Pelew” was a smart
little schooner of a hundred and fifty tons, could sail like a water
witch, and was a right staunch little craft. We shipped three deck
hands, one a young Danish seaman, who had cleared out from an
English ship at Brisbane, and two Kanakas. The Dane was a smart,
active young fellow, his only drawback being that he could not speak
a word of English, but it was evident he would soon learn. The
Kanakas were two splendid types of the Solomon Islanders, they
were sharp, intelligent men and could speak “pigeon” English. In
their younger days they had been slaves on a Queensland sugar
plantation, but for the last two years they had been on one of the
missionary schooners cruising among the Pacific Islands. They took
life very merrily, and were always laughing, no matter what had to be
done—they got some fun out of it. Work was no trouble to them, and
when there was no work going on they would wrestle with each
other, tumbling each other about until the perspiration rolled off them,
but they never lost their tempers over it, but would finish up with a
hearty laugh. Sometimes they would get the young Danish sailor to
wrestle with them, but they could do just what they liked with him, he
was muscular and strong, but they were slippery as eels, and twisted
and twirled as though there was not a bone in their bodies, and
always slipped out of his fingers before he could get a grip on them.
It was great fun to Captain Brown and me to see the Kanakas,
Tombaa and Panape, trying to teach Neilson, the Dane, to speak
English, and Neilson trying to teach them Danish. That seemed the
only thing they could not get any fun out of. At last Panape gave it
up, and would not have it at any price.
“That no tam good,” said he, shaking his head. “Good fellow white
man—speak Englis’—no that allee samee you. You no takee allee
same good fellow captain—good fellow, mate?”
“No,” said Neilson in English.
“You no tam good, then,” said the Kanaka. “All good fellow speak
Englis’. Me good fellow—me speak Englis’. Tombaa, he good fellow
man, too—he speak allee samee missiony man, he teach us to say
prayer to ‘Big Fellow Master’ (God), prayer belong sleep, prayer
belong get up. Tombaa you speak white fellow commandments.”
I drew nearer to them, anxious to hear a Kanaka’s version of the
ten commandments. Tombaa stood up, and throwing his chest out
like a proud turkey cock, he delivered the following version:—
The Ten Commandments in Kanaka.
I. Man take one fellow God, no more.
II. Man like him God first time, everything else behind.
III. Man no swear.
IV. Man keep Sunday good fellow day, belong big fellow
Master.
V. Man be good fellow longa father, mother belonga him.
VI. Man no kill.
VII. Man no take him mary belonga ’nother fellow man.
VIII. Man no steal.
IX. Man no tell him lie ’bout ’nother fellow man.
X. ’Supose man see good fellow something belonga
’nother fellow man, he no want him all the time.
 I was much amused at their interpretation, what it lacked in length
was made up by the clear definition of the meaning of the ten
commandments, and these two lived up to it.
We left Cooktown with a general assortment of cargo for
Townsville, and a few deck passengers. The wind being fair and the
weather fine, we made the passage in fifty-four hours, anchoring
inside Magnetic Island. Our cargo and passengers were soon
landed, and the schooner loaded for Port Moresby, New Guinea. The
cargo consisted of cloth, prints, calicoes, ribbons of all sorts and
colours, tobacco (horrid stuff), spirits, axes and various joinery tools,
etc., and some agricultural implements. We also had four
passengers—German officials—going to the German settlement,
north-east New Guinea.
We left the port at sunrise. The weather was fine, one of those
lovely tropical days when the sky blends its prismatic hues and the
easterly breeze, as it whistles through the shrouds, brings new life
and energy into one’s veins. The sea all around was covered with
silver-crested waves and as the little “Pelew” cut her way through the
sparkling waters she sent them like showers of jewels along her
painted sides. What a joy it was to me to be once more on the
ocean, to feel once more the motion of the vessel beneath my feet,
and to quaff the salt breeze that was like the wine of life. We had a
delightful passage, but owing to the numerous reefs and shoals we
were kept constantly on the lookout. These seas require the most
careful navigation, and I was surprised to find that Captain Brown
seemed quite at his ease among the reefs, although, when I
mentioned this and asked him about his life in these regions, I could
never get any very definite answers from him. However by putting
two and two together, from his chance remarks, I came to the
conclusion that he had been what is known as a “blackbird catcher,”
an “island scourger,” a “dealer in living ebony,” or a “sandlewood
thief.”
We made the passage to Port Moresby in five days. As soon as
we anchored in the bay three native crafts came off for our cargo, the
agent who was in the first boat seemed half a savage himself, and
had a most repulsive face. Captain Brown gave orders that no one
was to leave the ship on any pretext whatever, except the German
passengers, and they did not seem to like the job either, but that was
what they had come out for. No natives were allowed to come on
board. Their appearance was not very inviting, they were quite
naked, with the exception of a strip of pounded bark or cocoanut
fibre round their waist, their woolly heads were decked with shells
and tufts of grass, while round their necks each had a necklace of
shark’s teeth. Though fine, well-built, powerful looking fellows, their
features were not what we should call handsome, as their foreheads
are low and retreating, the face broad, the cheek-bones prominent,
the nose flat and the lips thick. We heard that there was an English
missionary living amongst them and doing a good work.
After delivering what goods we had for the store-keeper, we
received orders to proceed to Gaurdalcana in the Solomon Islands,
and deliver the balance to the store-keeper there.
Captain Brown then told me that the natives of the Solomon
Islands were cannibals, “so you had better be careful while we are
amongst these islands, and,” he continued, with a sly twinkle in his
eyes “you have to be very cautious in dealing with them, for they are
very partial to roast sailor. I had a terrible experience on one of the
islands some years ago. I was in a smart little brig, cruising among
the Islands. We were out on a blackbird (native) catching expedition.
We sailed into the bay at the south-east point of San-Christobal. The
brig ‘Carl’ of blackbird notoriety, had been there a few times, and
after getting a number of the natives on board to trade as they
thought, they had been invited into the saloon, and their eyes were
dazzled by the beads and toys and other things spread on the table.
Unsuspecting of any treachery they stayed until the gentle rolling of
the vessel caused them to ask with some surprise what it meant, by
this time the ship was well under way, and fast leaving San-
Christobal behind them. They tried to rush on deck, but found
themselves covered with the rifles of some of the ship’s crew, they
were soon overpowered and made prisoners and put into the hold
with others who had been lured to the vessel by the same device—
all to be sold as slaves to the North Queensland planters—but we
were not aware of this at the time.
“Well, as we drew up towards the head of the bay we suddenly
grounded on a reef, and while we were rushing about backing and
filling the sails, the natives swam off in hundreds and boarded the
vessel on all sides. We let go the ropes and seized whatever we
could lay our hands on to defend ourselves, but in a minute three of
our men were beaten to death with clubs. The captain was aft by the
wheel, and as soon as I saw the natives climbing over the rail I drew
my knife and sprang aft near him, and together we fought like
demons. But the copper-coloured fiends thronged round us, and one
big fellow at last got a blow in with a club that laid the captain
senseless on the deck. But his triumph was short, and mine too, for I
ripped him open with my knife, and the next minute was knocked
senseless on the deck myself. When I came to, I was on the floor of
a hut on shore, trussed like a fowl, with my arms and legs bent
behind me and lashed together. I struggled and twisted to get my
hands free, but it was no use, I could not do it. I raved and shouted
for some one to come and put me out of my misery. At last, as if in
answer to my cry, one of the women came and looked in, and seeing
me struggling, she picked up a club, and smashed me on the head
with it, and again I became senseless. The next thing I remembered
was being rolled over and over and my flesh being pinched by two or
three natives. After jabbering among themselves for a few minutes
they left me, and directly afterwards I heard the captain’s voice
shouting not far off, and a lot of jabber among the natives. I could not
see what was going on, but I knew that they were taking the poor
fellow to kill and roast him. I tore at my bonds, until the lashings cut
into the flesh. Suddenly a horrible yell burst on my ears, and I knew it
was the captain’s death cry. I shook like a leaf, and the perspiration
rolled off me like raindrops. I was on the rack with torture, knowing
full well what was before me, and that at any minute my turn might
come. I swooned away with horror at the thought, to be brought to
later by a burning stick being thrust into my face. I saw four of the
devils were in the hut, and a whole crowd outside. They put a small
spar through my arms, and two of them lifted me up between them,
like a Chinaman carrying a load. As they carried me along towards a
large fire in the middle of a clearing, near a large hut, like a meeting
house, my stomach and face were scraping the ground, and, oh!
God, what a terrible sight met my eyes. There just in front of me was
the roasting body of the poor skipper. He had been a bad devil in his
time and many an islander had suffered at his hands, but they had
got their revenge on him for it.
“The head man or chief now spoke to a big powerful savage, and
the latter approaching me with a large knife, was about to plunge it
into me to rip me open, when the head man, who was jumping about
before me, suddenly fell forward on his face and lay still. The others
looked on and shouted. Then some of the elder ones, seeing there
was something wrong, walked up to the prostrate chief, and touched
him. Finding he did not move, they turned him over, but he was
dead. I thought they would fall on me at once when they realized
this, but they only set up a great wail and beat their breasts with their
hands. Then two of the old men spoke up, and all was quiet. After
they had done speaking several of the men came to me, and I
thought my last moment had come, but, to my surprise, they gently
untied my hands and feet. For a few minutes I was unable to stand,
but as soon as I could, one of the old men picked up the spear and
club of the dead chief, placed them in my hands, and pointed to the
hills. I was not long in taking advantage of my freedom, and made
tracks at once. I could hardly believe that I was free, and expected
every minute to hear them coming after me.
“Why I had been spared was a mystery to me then, but I
afterwards learned that they released me through some superstitious
fear, and a belief that the spirit of their dead chief had entered into
me, had I been so minded they would have made me chief of the
tribe; this they tried to make me understand when the old man
placed in my hands the spear and club belonging to the dead chief. It
would have made no difference to me had I known, all I wanted was
to put as many miles as possible between the cursed place and
myself.
“I remained in hiding for a couple of days up among the hills, and,
strange to say, I never saw a single native come near to the place
where I was. Another thing I noticed in my wanderings was the
absence of children. I don’t remember seeing a single youngster. As
a rule there are plenty of them knocking about on most of these
islands, so I came to the conclusion that this was an island where it
is the custom for nearly all the children of both sexes to be killed by
their parents, perhaps eaten, too. I lived on bananas, cocoanuts, and