Multiple Sclerosis and Related Disorders (2014) 3, 413–415

Available online at www.sciencedirect.com

journal homepage: www.elsevier.com/locate/msard

CASE REPORT

Case report of multiple sclerosis diagnosis

in an 82-year old male
Emma Fostern, Benjamin K-T. Tsang, Olga Skibina, Anthony Kam,
Elsdon Storey

The Alfred Hospital, Commercial Road, Prahran, VIC 3181, Australia

Received 31 March 2013; received in revised form 11 September 2013; accepted 6 November 2013

KEYWORDS Abstract
Late onset; An 82-year old male, with no significant past medical history, presented with a subacute right
Multiple sclerosis; foot drop in the setting of a 14-month history of generalised weakness, highly-responsive to
Magnetic resonance steroids. Temporal artery and vastus lateralis biopsies were normal. Vasculitic screen and
imaging; inflammatory markers were normal. Lumbar puncture revealed elevated cerebrospinal fluid
Natalizumab;
(CSF) protein without oligoclonal bands. Visual evoked response (VER) was normal. Magnetic
Central nervous
resonance imaging (MRI) of his lumbar spine showed compression of exiting L5 nerve root. He
system;
Demyelination had three cerebral MRI scans spaced over the 12 month period, which showed a progressive
increase of T2 and fluid attenuated inversion recovery (FLAIR) hyperintense lesions consistent
with active demyelinating plaques. He was treated with intravenous methylprednisolone 1 g
daily for three days with a weaning regimen of oral prednisolone, resulting in a full return of
power and a resolution of his right foot drop. He was diagnosed with late-onset multiple
sclerosis (LOMS), and was treated with monthly natalizumab. A literature review of LOMS is
discussed.
& 2013 Elsevier B.V. All rights reserved.

We report the case of an 82 year-old gentleman, who is the
oldest person to be diagnosed with multiple sclerosis
according to the Australian Multiple Sclerosis Registry
(personal communication, Tomas Kalincik, MSBase founda-
tion), and one of the oldest reported in the international
literature (Takeuchi et al., 2008; Kis et al., 2008).
He was admitted to our centre for workup of a subacute right
foot drop, in the setting of a 14-month history of generalised
n
Corresponding author. Tel.: +61 3 9076 2000; fax: +61 3 9076 5075.
E-mail address: dr.ecfoster@gmail.com (E. Foster).
weakness. He had no significant past neurological, medical or
family history, and until recently was completing ironman
distance sporting events. His initial complaint was difficulty
completing a long distance swim race, and from that time,
ongoing generalised weakness and lethargy. Four months later,
he developed intermittent bilateral temporal-mandibular pain.
Temporal artery biopsies and a lateral thigh biopsy at this time
were normal, and the symptoms resolved with pulsed steroids.
His lethargy, generalised aches and weakness gradually returned
over a 12-month period, corresponding to a weaning steroid
dose. He then developed a right foot drop, and was referred to
our centre for an opinion regarding the underlying disease

2211-0348/$ - see front matter & 2013 Elsevier B.V. All rights reserved.
http://dx.doi.org/10.1016/j.msard.2013.11.002
414 E. Foster et al.

process. Examination revealed 2/5 power for dorsiflexion, presentation or within 1 year of symptom onset (Kis et al.,
plantar flexion, ankle inversion and eversion. Nerve conduction 2008). The most common misdiagnoses include unspecified
studies (NCS) showed normal right peroneal and tibial com- inflammatory process of the central nervous system (CNS),
pound muscle action potentials without focal slowing or cervical myelopathy, polyneuropathy and stroke (Kis et al.,
conduction block and lower limb sensory potentials were also 2008). Our patient's diagnosis was made 14 months after initial
normal. Electromyography in the lower limbs demonstrated symptom onset, delayed while differential diagnoses including
only minor loss of motor units in the right sciatic innervated vasculitis, sarcoidosis and CNS lymphoma were considered. His
muscles without signs of denervation suggesting the possibility vague, generalised symptoms could account for any of the
of an upper motor neuron process to produce these findings. above, however, extensive testing for infectious, neoplastic and
Vasculitic and autoimmune screen were essentially normal. vasculitic processes was unremarkable. The only consistent
These included p-ANCA, c-ANCA ‘indeterminate’ in the pre- abnormal finding was the ever-increasing number of incomplete
sence of antinuclear antibodies; myeloperoxidase antibody and ring-enhancing lesions on cerebral MRI scans consistent with an
proteinase 3 antibody normal, rheumatoid factor 47 (nor- active demyelinating process and hence, a diagnosis of LOMS
malo11), ANA weakly positive, speckled, and titre 160 (normal was favoured.
0–100), double-stranded DNA negative, ENA panel, including
ENA-SS-A, ENA-SS-B, ENA-RnP, ENA-Sm, ENA-Scl70, ENA-Jo1,
were negative, and transglutaminase antibodies IgAo1. In
terms of infective screen, tests for HIV, tuberculosis and syphilis
were negative. Lumbar puncture revealed CSF which was clear
and colourless, glucose 3.8 (normal), protein 0.67 (elevated,
normal range 0.15–0.40), oligoclonal IgG identical banding
pattern to serum, therefore unlikely to be intrathecal in origin;
polymorphs nil, erythrocytes nil, lymphocytes 2, nil growth.
Cytospin showed mild increase in mature lymphocytes and
scattered monocytes, with no evidence of malignancy. Visual
evoked responses were normal. Lumbar spine MRI showed
compression of exiting L5 nerve root. He had three cerebral
MRI scans spaced over the 12 month period (Figs. 1 and 2).
These showed a progressive increase of lesions consistent with
active demyelinating plaques, and fulfilled the current McDo-
nald MS diagnostic criteria. He was diagnosed with relapsing
remitting multiple sclerosis.
He was treated with intravenous methylprednisolone 1 g
daily for three days with a weaning regimen of oral Figure 1 Sagittal FLAIR T2 image taken prior to treatment
prednisolone, and had full return of power, with resolution shows multiple hyperintense lesions with long axis perpendicu-
of his right foot drop. He was commenced on monthly lar to the corpus callosum.
natalizumab, which in Australia is approved as a first line
disease modulating treatment, and was chosen based on the
patient’s high disease activity and possible compliance
issues with self-administered daily injections.
Multiple sclerosis (MS) is the most common neurological
demyelinating disease affecting young adults (Takeuchi et al.,
2008; Polliack et al., 2001), typically diagnosed between 20 and
40 years of age (Takeuchi et al., 2008; Qiu et al., 2010), with
almost twice as many females affected as males (Thompson
et al., 1997). Adult onset MS (AOMS) is defined as MS diagnosed
between the ages of 16 and 50 (Tremlett and Devonshire,
2006). Late onset MS after age 50 (Kis et al., 2008) and some
authors define very late onset MS as MS diagnosed after age 60
(Qiu et al., 2010). Only 4.6% of MS cases are diagnosed in those
over age 50 (Polliack et al., 2001), and only 0.45% in those over
60 years of age (Delalande et al., 2002). As Tremlett and
Devonshire remark(Tremlett and Devonshire, 2006), “while the
onset of multiple sclerosis in older adults is not unheard of, it is
still relative unusual”, and certainly a diagnosis at age 82 is
rare. A literature search by the authors have found mention of
only two patients diagnosed in their 80s; one at 82 (Kis et al.,
2008) and at 87 (Takeuchi et al., 2008).
Perhaps because it is rare, a diagnosis of LOMS is frequently Figure 2 Axial T1 post gadolinium image taken before treat-
delayed while differential diagnoses are considered (De Seze ment shows circumscribed T1 hypointense lesions, some with
et al., 2005). Forty per cent of LOMS diagnoses are delayed on incomplete leading edge enhancement typical of active
average 3 years, compared to AOMS which is diagnosed at initial demyelination.
Multiple sclerosis diagnosis
Clinical features of LOMS differ from AOMS. Patients with
LOMS experience more motor symptoms compared with
AOMS, with rates of 90% and 67% respectively (Kis et al.,
2008). Given this data, it is not surprising that motor
symptoms are the most common presenting complaint of
LOMS, accounting for 63.3% of initial presentations, com-
pared with sensory symptoms which accounted for 30%
(Polliack et al., 2001). Patients with LOMS experience less
visual symptoms, residual signs of optic neuritis, and
dysarthria, compared with AOMS patients (Kis et al.,
2008). Sensory symptoms, ataxia, oculomotor signs, cogni-
tive disorder and fatigue occur equally between the two
groups (Kis et al., 2008). Our patient's initial presentation
was with subacute motor symptoms and generalised fatigue,
in keeping with the current literature findings of LOMS
clinical features.
There are conflicting reports as to whether disease
progression in LOMS differs from AOMS. One study shows
that the majority of LOMS patients (83%) experience a
primary progressive (PP) course, compared with AOMS, the
vast majority (94%) of whom experience a relapsing-
remitting (RR) course (Kis et al., 2008). Another study found
that all those aged over 54 had a PP course and that LOMS
was associated with a faster progression to disability
(Polliack et al., 2001). In contrast, Tremlett & Devonshire
(Tremlett and Devonshire, 2006) report that time to mod-
erate disability between LO & AO groups are similar,
suggesting disease course may be set relatively early in
both groups.
In conclusion, we present a very interesting and rare case
of LOMS in an 82 year-old gentleman. Although he has some
atypical presenting complaints, the most likely underlying
415
cause is multiple sclerosis. The case illustrates that Clin-
icians should be aware of possible active demyelinating
disease in older people when considering their diagnostic
and treatment approach.
Conflict of interest
Authors declare no conflict of interest.
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