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review of MS mimickers

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PostPosted: Thu Oct 26, 2006 4:32 pm    Post subject: Reply with quote

This is from a stats class...that's why I deleted it initially. It doesn't seem to be a stat class for medical students specifically. So, I don't know how accurate the information is. Homework's 1 to 4 have nothing to do with medicine.

At least some of the numbers seem correct. If there could be ANY pre-med students in the class, than there should have been at least some effort to make sure that the information is correct. And there almost invariably ARE pre-med students in stat classes.

But, be forwarned that this COULD BE AN UNRELIABLE SOURCE.
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PostPosted: Sat Nov 04, 2006 4:49 pm    Post subject: Reply with quote

There's also now a blood test for neuromyelitis optica, which is either a mimicker or a variant of MS.
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PostPosted: Sat Jan 20, 2007 3:07 pm    Post subject: (Abstract) Fabry disease mimicking MS Reply with quote

From PubMed, January 20, 2007:

Clin Neurol Neurosurg. 2007 Jan 16

Fabry disease mimicking multiple sclerosis

Saip S, Uluduz D, Erkol G.
Department of Neurology, Istanbul University Cerrahpasa Medical Faculty, Istanbul, Turkey.

Fabry disease is an X-linked recessive lysosomal storage disorder resulting from the deficiency of alpha-galactosidase. This disease causes endothelial vasculopathy and affects multiple organ systems. Hemizygous male patients represent the classical renal, cardiac and neurological symptoms of disease. Heterozygous female carriers are frequently asymptomatic, but cerebrovascular events in females are as frequent as in males.

Even if rarely seen, neurological damage is an important cause of morbidity. Severe neurological signs that are due to multifocal small vessel occlusions may be present without major thrombosis.

In this report, we present a 33-year-old female patient with recurrent neurological deficits secondary to multifocal small vessel involvements. The case had previously been misdiagnosed as multiple sclerosis. Cerebral MRI revealed hyperintense lesions located in bilateral thalamus, supratentorial areas, and left cerebellum. Laboratory and radiological investigations were performed for differential diagnosis, but the etiology could not be identified.

During follow-up period, skin lesions and proteinuria were detected. The dermatological, neurological, laboratory, and radiological findings were all suggestive of Fabry disease and the diagnosis was confirmed by subsequent enzyme assays.

Fabry disease should be considered in young patients with unexplained stroke-like episodes, especially in those who have infarction in the vertebrobasilar arterial system, angiokeratomas, and proteinuria.

PMID: 17234336
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PostPosted: Wed Mar 14, 2007 2:10 pm    Post subject: (Abstract) Differential diagnosis of MS Reply with quote

From PubMed, 3/14/07:

Neurologist. 2007 Mar;13(2):57-72

The Differential Diagnosis of Multiple Sclerosis

Rolak LA, Fleming JO.
From the Marshfield Multiple Sclerosis Center, Marshfield Clinic, Marshfield, Wisconsin; and Neurology, University of Wisconsin, Madison, Wisconsin.

OBJECTIVE: This article will discuss the diagnosis of multiple sclerosis (MS), with particular attention to differentiating it from other diseases that can mimic it.

METHODS: We reviewed our own data, as well as the published experience on the differential diagnosis of MS and the most common errors leading to misdiagnosis.

RESULTS: Psychiatric diseases are mistaken for multiple sclerosis more often than any other conditions. Other multifocal illnesses or white-matter diseases are seldom confused with multiple sclerosis.

CONCLUSION: Neurologists are most likely to misdiagnose multiple sclerosis in patients who have psychiatric problems or who have uncommon presentations of common diseases such as migraine, stroke, or neuropathies.

PMID: 17351525
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PostPosted: Tue May 29, 2007 1:50 pm    Post subject: (Abstract) Differential dx of MS Reply with quote

From PubMed, May 29, 2007:

Int Rev Neurobiol. 2007;79C:393-422

Differential Diagnosis of Multiple Sclerosis

Fadil H, Kelley RE, Gonzalez-Toledo E.
Department of Neurology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71103, USA.

There are a number of illnesses that can mimic multiple sclerosis (MS). This pretty much includes any pathological process that can reflect injury to the central nervous system either on a transient or progressive basis.

Typically, MS presents itself in individuals in their teens up to their late 30s. On occasion, however, one can see MS present in patients in their 60s. However, in retrospect, many of these patients might have had subtle manifestations of MS in their younger years.

Visual obscuration or visual loss can be a manifestation of retinal ischemia, retinal migraine, or optic neuritis which might or might not evolve into a clinical picture compatible with MS. Cranial neuropathy, long tract signs, sensory disturbance, and/or gait ataxia can be related to a number of different processes such as illicit drug use, neurosarcoidosis, neuro-Behcet's disease, neuroborreliosis, HIV-related disease, neurosyphilis, vascular occlusive disease including vasculitis, connective tissue disorders, acute disseminated encephalomyelitis (ADEM), idiopathic transverse myelitis, neuromyelitis optica (NMO), or tropical spastic paraparesis.

In addition, a constellation of symptoms, with questionable objective findings, along with normal MRI imaging, normal CSF results, and normal evoked response testing, when indicated, might identify a conversion disorder or possibly malingering.

There are now established criteria for the diagnosis of MS, but initial presentations can be less than "textbook" in nature. With the advent of immunomodulating therapy, it has become more important to diagnose MS more effectively earlier on in the course of the illness.

Prior to specific therapy for MS, astute clinicians did not necessarily move with alacrity to establish the diagnosis in patients with subtle or transient manifestations. This was in recognition that little could be offered to alter the course of the illness and a number of patients might never experience further problems if they were lucky enough to have their illness go into permanent remission after one minor exacerbation.

PMID: 17531852
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PostPosted: Tue Jul 24, 2007 1:42 pm    Post subject: Reply with quote

An article on optic disc pallor, showing the importance of ruling out alternative causes other than optic neuritis.
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PostPosted: Fri Jul 27, 2007 1:46 pm    Post subject: (Abstract) Hughes syndrome [antiphospholipid syndrome] Reply with quote

From PubMed, July 27, 2007:

Clin Experiment Ophthalmol. 2007 Jul;35(5):496-8

Hughes syndrome

Sivaprasad S, Gregor Z.
Moorfileds Eye Hospital, London, UK.

Antiphospholipid syndrome, also known as Hughes syndrome, is a recently described entity that mimics symptoms of other diseases such as multiple sclerosis. It is a potentially life-threatening autoimmune disorder where the body produces antibodies directed against phospholipids and phospholipid-binding proteins. Herein a patient with successive ocular vascular events associated with antiphospholipid syndrome is presented.

PMID: 17651260
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PostPosted: Sun Apr 13, 2008 10:50 am    Post subject: (Abstract) Connective tissue diseases mimicking MS Reply with quote

I'm moving this posting to this thread.

From PubMed, June 16, 2007:

Rheumatol Int. 2007 Jun 15

Neurological manifestations of connective tissue diseases mimicking multiple sclerosis

Pelidou SH, Giannopoulos S, Tzavidi S, Tsifetaki N, Kitsos G, Stefanou D, Kostadima V, Drosos AA, Kyritsis AP.
Department of Neurology, University of Ioannina School of Medicine, University Campus, Ioannina, 45110, Greece,

The objective of the study was to analyze retrospectively the clinical, laboratory and imaging findings of multiple sclerosis (MS), such as the manifestations in a cohort of 132 patients referred to the neurology in and outpatient clinic.

The proposed clinical and laboratory diagnostic criteria for MS and connective tissue disorders were systematically assessed in 132 consecutive patients. Cerebrospinal fluid serology and brain or spinal cord MRI were studied in all cases. In patients suspected for connective tissue disorder, schirmer test, rose bengal staining and biopsy of minor salivary glands were performed.

A total of 115 (87%) patients were diagnosed to have definite MS, while 17 (13%) were diagnosed to have connective tissue disorder. Positive neurological and MRI findings were observed in both groups. The majority of patients with connective tissue disorder demonstrated extra-neurological manifestations like Raynaud's phenomenon, arthritis, livedo reticularis, purpura and presence of multiple autoantibodies in their sera.

All patients with MS should be screened systematically for connective tissue disorder. In the absence of pathognomonic clinical and laboratory findings, the diagnosis of MS is a diagnosis of exclusion.

PMID: 17571265
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PostPosted: Sun Oct 05, 2008 1:04 pm    Post subject: Reply with quote
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PostPosted: Thu Mar 05, 2009 8:47 am    Post subject: Article on disorders mimicking MS by Patricia K. Coyle, MD Reply with quote

This article appeared in 2006 in the Johns Hopkins Advanced Studies in Medicine:
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PostPosted: Fri May 08, 2009 2:32 pm    Post subject: Reply with quote

As for the causes of INO...
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PostPosted: Thu Feb 04, 2010 1:49 pm    Post subject: Reply with quote

antiphospholipid syndrome...a blood clotting disorder
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PostPosted: Thu May 06, 2010 4:47 pm    Post subject: (Abstract) Rare infections mimicking MS Reply with quote

From PubMed, May 5, 2010:

Clin Neurol Neurosurg. 2010 May 1. [Epub ahead of print]

Rare infections mimicking MS

Brinar VV, Habek M.

University of Zagreb, School of Medicine and University Hospital Centre Zagreb, Department of Neurology and Refferal Center for Demyelinating Diseases of the Central Nervous System, Zagreb, Croatia.

The diagnosis of multiple sclerosis (MS), despite well defined clinical criteria, is not always simple. On many occasions it is difficult to differentiate MS from various non-MS idiopathic demyelinating disorders, specific and infectious inflammatory diseases or non-inflammatory demyelinating diseases.

Clinicians should be aware of various clinical and MRI "red flags" that may point to the other diagnosis and demand further diagnostic evaluation. It is generally accepted that atypical clinical symptoms or atypical neuroimaging signs determine necessity for broad differential diagnostic work up.

Of the infectious diseases that are most commonly mistaken for MS the clinician should take into account Whipple's disease, Lyme disease, syphilis, HIV/AIDS, Brucellosis, HHV-6 infection, hepatitis C, mycoplasma and Creutzfeld-Jacob disease, among others.

Cat scratch disease caused by Bartonella hensellae, Mediterranean spotted fever caused by Riketssia connore and Leptospirosis caused by different Leptospira serovars rarely cause focal neurological deficit and demyelinating MRI changes similar to MS.

When atypical clinical and neuroimaging presentations are present, serology on rare infectious diseases that may mimic MS may be warranted.

This review will focus on the infectious diseases mimicking MS with presentation of rare illustrative cases.

PMID: 20439131

The abstract can be seen here.
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PostPosted: Fri Jul 16, 2010 5:40 pm    Post subject: Reply with quote

thanks for all this good information
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PostPosted: Sun Apr 17, 2011 12:14 pm    Post subject: (AAN) What can mimic MS on MRI? Reply with quote

Ditzy, you're welcome!

Presented at the AAN conference in Hawaii, April 9-16, 2011:

[8SM.001] Neuroimaging for the Practicing Neurologist: What Can Mimic MS on MRI?

Konstantin E. Balashov, MD, PhD

Program Description:

Few, if any, neurological disorders are currently evaluated without neuroimaging. As a result, practicing neurologists see more and more patients found to have white matter lesions on brain MRI. Is it multiple sclerosis (MS) or one of many other neurological disorders that can mimic MS both clinically and on MRI? Through lectures and case presentations, typical MRI features of MS and MS mimickers, e.g., neuroborreliosis, progressive multifocal leukoencephalopathy (PML), neuromyelitis optica (NMO), acute demyelinating encephalomyelitis (ADEM), will be reviewed. The usefulness and limitations of MRI in MS diagnosis will be discussed.


Saturday, April 16, 2011 6:30 AM

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PostPosted: Tue Nov 06, 2012 8:20 pm    Post subject: (Abst.) Moyamoya disease can masquerade as MS Reply with quote

From PubMed, November 2, 2012:

Neurologist. 2012 Nov;18(6):398-403.

Moyamoya disease can masquerade as multiple sclerosis

Dorfman LJ, Fischbein NJ, Woodard JI, Choudhri O, Bell-Stephens TE, Steinberg GK.

Departments of *Neurology and Neurological Sciences ‡Radiology §Neurosurgery †The Stanford Stroke Center, Stanford University School of Medicine, Stanford, CA.


Moyamoya disease (MM) is a rare disorder of the cerebral arterial circulation, whereas multiple sclerosis (MS) is a relatively common immune-mediated attack on central myelin. Despite the differences in pathogenesis, the 2 disorders share some clinical features which can lead to diagnostic confusion: both can affect young adults, cause intermittent neurological symptoms, and show multifocal abnormalities on brain imaging.


To emphasize the need for early consideration of MM in the differential diagnosis of MS-spectrum disorders.


Chart reviews and individual case analyses.


We present detailed descriptions of 3 patients with MM, and summary data on 8 additional cases, in which there was diagnostic confusion with MS, with delays in treatment ranging from 2 months to 19 years (median=4 y).


MM can be misdiagnosed as MS, leading to delay in correct treatment. We highlight the clinical and radiologic features which allow differentiation of these conditions early in the course, when treatment can have maximum benefit.


The abstract can be seen here.
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PostPosted: Mon Dec 03, 2012 11:28 am    Post subject: Reply with quote

This is a old study addressing MS misdiagnosis before mri was relied upon widely

Acta Neurol. Scand., 1988:78:39-44
Key words: multiple sclerosis; clinical diagnosis;
pathoanatomical diagnosis; optic nerve examination;
diagnostic errors.
A clinico-pathoanatomical study of
multiple sclerosis diagnosis
T. Engell
The Danish Multiple Sclerosis Register
ABSTRACT - The diagnosis of multiple sclerosis (MS) is clinical and verifiable at
post mortem. Neuropathological examination of 518 consecutive patients with clinically
definite MS revealed a correct diagnosis in 485 cases (94Vo). Clinical diagnosis
had been established by a neurologist in all cases. Erroneous diagnosis included a
variety of other neurological disorders. Also investigated was a randomly selected
series of 33 patients with a clinical diagnosis of probable MS: post mortem confirmation
of MS was obtained in circa 66%. for the remainder the error pattern was
similar to the above. Clinical diagnosis of definite MS was correct in 94% cases.
Laboratory tests and examinations have not radically improved diagnosis. Neuropathological
examination may occasionally fail to demonstrate MS plaques if the
optic nerves are not investigated.
Accepted for publication January 22, 1988
The diagnosis of MS is clinical, finally verifiable
postmortem. Although the most common of the
demyelinating diseases and usually with characteristic
clinical manifestations if observed over a
period, MS may occasionally be difficult to diagnose
in vivo. This is emphasized by the list of
diagnostic criteria finally proposed by the Schumacher
a) there must be objective abnormalities on
neurologic examination attributable to dysfunction
of the central nervous system;
b) on neurologic examination or by history there,
must be evidence or involvement of 2 or more
separate parts of the central nervous system;
c) objective neurologic evidence of central nervous
system disease must reflect predominantly
white matter involvement, i.e., fiber tract damage;
d) involvement of the neuroaxis must have
occurred temporally in one or the other of the
following patterns:
1) in two or more episodes of worsening, separated
by a period of one month or more, each
episode lasting at least 24 h;
2) slow or step-wise progression of signs and
symptoms, over a period of at least 6 months;
e) onset between 10 and 50 years of age inclusive;
f) the patients’ signs and symptoms cannot be
better explained by some other disease process, a
decision which must be made by a physician
competent in clinical neurology.
These criteria have subsequently been modified
(1-3). The etiology is unknown, but the pathogenesis
may involve immunoallergic mechanisms.
Pathoanatomically MS is characterized by the
formation of plaques of demyelination with gliosis.
On gross examination the lesions present as
rounded, well demarcated areas, the size of
which usually ranges from 3-15 mm (4), the
older foci being greyish or translucent, the more
recent pink.
The dissemination of plaques throughout the
neuroaxis is an essential feature, but there are
such predilection areas as the periventricular
region, the optic nerves and the spinal cord (5).
and there is a tendency to bilateral distribution
of plaques (4). The number of plaques varies
considerably: Brownell (6) found a total of 1594
histologically verified plaques in 22 cases of MS.
The maximum count of plaques was 225 and the
minimum 3. Fog reported on one cerebrum with
a number of 10-11 plaques in one hemisphere
section, and less than half in the other. Lunsden
(4) described 10 cases which after a rapid progressive
course showed a total of 482 plaques.
On microscopic examination demyelinisation
with relative sparing of axons is a cardinal feature.
Inflammatory cellular lesions are often conspicuous
in recent plaques, but absent in old
plaques where fibrillary fibrosis predominates.
Loss of myelin, the major component of white
matter, is a common sequela of a multitude of
conditions, many of which initially affect other
elements of white matter such as blood vessels,
glia and axons. Thus, myelin is frequently damaged
secondarily by neoplasia, trauma, infarct,
necrosis, abscess, anoxia, edema or haemorrhage
in addition to degeneration of overlying cortex
(7). It is therefore not surprising that other diseases
occasionally may mimic MS and erronously
lead to this diagnosis.
Material and methods
Clinically definite MS group
The series comprised neuropathological investigation
of 518 patients with a clinically diagnosed
definite MS established during their lifetimes.
They were identified from the Danish MS
register and data regarding those who had died
during the period 1965- 1986 were consecutively
collated from the Danish National Register of
Health. From this, all cases who had undergone
postmortem were extracted.
Primarily excluded were 5 cases with insufficient
clinical data to permit a definite MS diagnosis, 6
cases with macroscopic neuropathological examination
only or with the histopathological examination
confined to limited parts of the CNS were also
excluded in case possible MS plaques had been
overlooked. Finally, one case was excluded as the
diagnosis had been partly based on abnormal evoked
responses and, thus, could not be considered a
purely clinical diagnosis.
Clinically probable MS group
To form an impression of the validity of the
probable MS diagnosis and to illuminate the
occasional difficulties of in vivo MS diagnosis an
additional random series of 33 patients with the
clinical diagnosis probable MS was gathered for
the same period and in the same way.
In all cases the clinical diagnosis had been
established by a neurologist often during admission
to a neurological department. The neurological
and pathoanatomical findings were
reviewed by examination of the patients’ medical
reports and postmortem records by both the
author and independently by the chief neurologist.
This review led to the inclusion of 2 further
cases of clinically definite MS which would previously
have been considered separate disease
entities. One was originally diagnosed as neuromyelitis
optica, the other as morbus Schilder.
In addition, one clinically definite MS diagnosis
was changed because of the PM finding of a
compression of the spinal cord, but no macroscopically
or histologically visible plaques were
seen in the CNS. However, later re-examination,
demonstrated MS plaques in th optic nerves (the
only site) and thus, this case was also finally
included in the MS group. One clinically definite
MS was subsequently transferred to the clinically
possible group (Case 6).
Group 1. Clinically definite MS
The diagnosis of clinically definite MS was confirmed
by neuropathological examination in 485
of the 518 cases, while it was found erroneous in
33. Of these, 9 had brain tumours, other neurological
diseases were diagnosed in 18, and 6
had suffered miscellaneous other diseases (Table
Of the 485 verified MS patients 232 were
women and 253 were men, mean age at the
onset was 32 (range 11-58). Mean disease duration
was 21 (range 0.5-40). For the 33 erroneous
diagnoses (19 W, 14 M) the mean age
at onset was 35 years and the mean duration 16
Group 2. Clinically probable MS
In the randomly selected series of 33 (15 M, 18
W) clinically probable MS, the diagnosis was
confirmed by neuropathological examination in
Table I
The corrected post mortem diagnosis of 33 cases diagnosed as clinically definite MS in vivo
Other neurological diseases Nos. Brain tumours Nos. Miscellaneous Nos.
Ataxia hereditaria,
Ataxia hereditaria 0.p.
Atrofia cerebri (myelitidis
Atrofia corticalis cerebellaris
Atrofia olivo-pontocerebellaris
Encephalitis chronica
Encephalitis sequelae
(Mb. Little?)
Encephalopathia chronica
Meylopathia c. anaemia
perniciosae ( I )
Myelopathia chron. medullae
Polyneuropathia causa ignota
Syringomyelia et bulbiae (2)
Angioma arteriovenosum
Angioma racemosum
verminis cerebelli (3)
Angiomatosis medulla spinalis
et putaminis dext.
Astrocytoma cerebellaris
Haemangioma cerebri
Metastasis medulla spinalis
et cerebri
Oligoblastoma pontis
Arteriosclerosis medualla spinalis
cervicalis medulla oblongata et pontis I
Cholesteratoma intracranialis I
Compressio medulla spinalis ( 5 ' ) I
lnfactus cerebri hemispherii dxt. (6)
Haemorrhagia cerebri dxt. I
Osteomyelitis columna thoracalis I
Total 18 9 6
Numerals in () refer to case numbers. See also study for discussion of the diagnosis
21, with a mean age at onset of 37 years, (range
20-54 years) and mean duration of 19 years
(range 1-45).
In the 12 cases where PM evidence showed
diseases other than MS, the mean age at onset
was 40 years (range 30-55 years) and a mean
duration of 13 years (range 1-45); correct diagnoses
are given in Table 2.
Seven case studies illustrating the diagnostic
problems sometimes encountered in diseases with
disseminated neurological symptoms are given,
numbers in () beside diagnoses in Tables 1 and 2
are their case numbers.
Case studies
Case 1. Female, age 45. Developed dragging of
the right leg when tired, progressive difficulties
in walking. Age 48: decreased strength of upper
limbs. Age 51: periods of double vision. Increasing
incontinence. Confined indoors with progressive
paralysis of the lower limbs, can stand
only by the aid of two persons. Neurological
examination, age 62: mentally euphoric, dysarthric
speech, paralysis of upper limbs, paralysis
of lower limbs with arefexia and bilateral
Babinski. She died at the age of 67.
Clinical diagnosis: definite MS.
Neuropathological diagnosis: anaemia perniciosa
with myelopathia.
Case 2. Female, age 27. Developed parasthesiae
of the hands and upper limbs and decreased
strength of left lower limb. Half a year later
progressive gait disturbances and bladder trouble.
Neurological examination, age 31: nystag42
Table 2
The corrected post mortem diagnosis of I2 cases diagnosed as probable MS in vivo
Other neurological diseases Nos. Brain tumours Nos. Miscellaneous Nos.
Dementia praesenilis (Alzheimer) (7) 1 Astrocytoma cerebri 2 Arteriosclerosis cerebri I
Myelopathia spongiosa 1 Astrocyloma pontis I lnfarctus cerebri hemispherii dxt 1
Sclerosis amyotrophica lateralis I Lymfogranulomatosis benigna Boeck 1
Syringomyelia et bulbia 2 Metastasis ad columnam I
Total 5 3 4
Numerals in () refer to case numbers.
mus, decreased strength and dysaesthesia of the
hands, right-sided reflex preponderance. Abdominal
reflexes absent. Slight proximal paralysis of
lower limbs, dysaesthesia, bilateral Babinski and
spastic gait. Through remission and relapses, the
condition became dominated by gait disturbances
and bladder trouble. She died at the age of 32.
Clinical diagnosis: probable MS.
Neuropathological diagnosis: syringomyelia et
bulbiae, syndroma Arnold-Chiari.
Case 3. Male, age 47. Developed gait disturbances.
Age 49: another attack treated with
ACTH with considerable effect. Age 55: progressive
deterioration. Neurological examination:
circumduction nystagmus, slight paralysis of left
arm, bilateral spastic augmented tonus with leftsided
preponderance and bilateral hyperreflaxia,
bilateral dysdiadochochinesis, no stereognostic
sence in the upper limbs. Muscular atrophia of
the legs, bilateral hyperreflexia, clonus and
Babinski. Gait spastic, atactic. Walks only when
supported. He died at the age of 57.
Clinical diagnosis: definite MS.
Neuropathological diagnosis: angioma racemosum
vermis cerebelli, compressio medullae
Case 4. Male, age 24. Difficulties moving the left
leg, dizziness when changing position. Neurological
examination: right-sided abducens paralysis,
nystagmus, slight facial paralysis. Atrophia of
the right side of the tongue with fasciculations.
In upper and lower limbs left-sided reflex preponderance.
Electromyography: deneration of
the right facial muscles. EEG: normal. Vertebral
angiography: normal. Age 25: progressive deterioration.
Repeated cerebral CT-scans normal,
repeated spinal fluid examinations normal.
Cisternography: normal. He died at the age of
Clinical diagnosis: probable MS.
Neuropathological diagnosis: astrocytoma pontis.
Case 5. Female, age 53. Debut with optic neuritis.
Age 62: progressive paralysis and attacks of
urinary retention. Ocular and neurological examination:
secondary atrophia of the optic nerves
and internuclear ophtalmophlegia. Nystagmus of
central origin. Bilateral hypotonia and areflexia
of lower limbs, bilateral Babinski. Myelography:
normal. Age 70: confined to wheelchair, permanent
urinary catheter. Died in hospital after sudden
loss of consciousness.
Clinical diagnosis: definite MS.
Neuropathological diagnosis: compression of the
medulla caused by discus degeneration in lumbar
columna. No demyelinating areas or MS plaques.
Optic nerves not investigated.
Discussion. The optic nerve atrophia, the internuclear
ophthalmoplagia and the nystagmus cannot
be explained by the neuropathological findings.
This patient may in addition to her spinal
lesion have had MS which remained undiagnosed
because the optic nerves were not examined.
Case 6. Female, age 34. Attack of paraesthesia
of the right hand with remission. Age 37: admitted
to neurological department with paraesthesia
of the hands, co-ordination disturbances of all
limbs, sagging of the left corner of the mouth,
headache and tiredness. Neurological examinoMS
tion: paralyses of left side of the mouth, slight
paralyses of left arm with dysdiadochochinesis
and discoordination. Left abdominal reflex
absent. Reflex preponderance of left lower limb.
A passing episode of nystagmus was noted. The
condition remitted in a few days. She died at the
age of 55 years of a pulmonary embolus.
Clinical diagnosis: probable MS.
Neuropathological diagnosis: infarctus cerebri
hemispherii dxt.
Case 7. Female, age 51. Back pain in the lower
limbs, mainly the left. Periods of paraesthesiae
of the hands and gait disturbances with coordination
trouble. Neurological examination:
mentally euphoric. Slight eye motility disturbances.
Normal upper limb and abdominal
reflexes, decreased strength in lower limbs,
reflexes and sensibility normal. Gait unstable
atactic. Some remission during stay in hospital.
She died at the age of 56.
Clinical diagnosis: probable MS.
Neuropathological examination: dementia praesenilis
The present study is, to the knowledge of the
author, the first large series of MS cases in which
the clinical and pathoanatomical findings have
been compared. The Mayo Clinic reported 14
clinically diagnosed cases of whom 13 were confirmed
by subsequent neuropathological examination
(8). Raine (7) has suggested the frequency
of erroneous diagnosis in MS to be in the range
of 5-10%. In the present study diagnosis was
correct in 94% of 518 cases.
The present series was selected from all Denmark
and, thus, represents the diagnostic work
of severeral neurological clinics and departments
of pathology.
The degree of uniformity and consistency
with which the clinical definite diagnosis has
been used by different neurologists has been
commented upon previously (8), and is emphasized
in the present study by the necessity for
only 3 changes of diagnosis. In 22/33 cases of
probable MS, the diagnosis was confirmed by
post mortem.
It is noteworthy that neither age at onset nor
disease duration differed significantly in patients
with clinically probable MS, in the first group
with proven MS, and in those who were erroneously
diagnosed. In the 12 clinically probable
MS found to have suffered other diseases,
however, the age of 40 years at onset was significantly
higher and disease duration of 13 years
shorter than for the other groups. This indicates
that diagnostic difficulties occur more frequently
in late onset diseases.
Differential diagnosis between MS and other
neurological diseases may occasionally be difficult,
especially if the patient is observed over a
short period; Disseminated neurological symptoms
in different neurological diseases may mimic
one another. In the total material of patients
with clinically definite or probable MS, most of
the diagnostic failures were due to other neurological
In recent years, several laboratory tests have
been introduced to support the clinical diagnosis
of MS, though most of them after the period
covered by this study. A diagnostic specificity of
100% has been claimed for the evoked potentials
test in MS patients (9). The results of the present
study argue against such specificity. It has also
been demonstrated that this specificity is in complete
because abnormal evoked potentials may be
encountered in such conditions as herediatary
ataxies, neurosyphilis, sarcoidosis and vitamin
B,, deficiency (8).
The presence of oligoclonal banding in cerebrospinal
fluid (CSF) has been reported in 94-
54% of patients with definite MS, the last given
figure clearly indicating a lack of sensitivity (10,
11); the specifity is further diminished by the test
proving positive in neurosyphilis, SSPE,
Guillain-Barrk syndrome, epilepsia and acute cerebrovascular
disease (8). It should perhaps be
mentioned that, in the present series, one patient
with MS plaques only in the optic nerves had
negative oligoclonal banding. Conversely, one
patient with encephalomyelo-radiculitis showing
diffuse demyelinisation without the occurrence
of MS plaques proved at postmortem to have
oligoclonal bands in the CSF.
Radiological examinations by computerised
tomography or technesium brain scintigraphy
have been extensively tried in MS, but give a high
rate of false negative results, when, for example,
a single large MS plaque falsely suggests a
tumour diagnosis (12-15).
NMR testing seems more promising, though its
sensitivity and specificity have yet to be ascertained
The diagnostic method of reference in MS is
the neuropathological examination. The existence
of a single or a few MS plaques might well
be overlooked on routine postmortem in the case
here described, where MS plaques were found
only in the optic nerves. Gartner (19), Ulrich (20)
and Toussaint (21) found optic nerve affection in
nearly 100% of MS cases. It is suggested that
routine examination of the optic nerves would
increase the reliability of the pathoanatomical
In the present study clinical diagnosis of MS
proved correct in 94% of a Danish MS population,
a validity exceeding any of the paraclinical
tests currently in use. However clinical diagnosis
of definite MS may be first obtained only after
years of observation in this protracted disease,
and some of the present laboratory tests, even
with their inherent imperfections, may be considered
useful supplementary procedures in the early
diagnosis of MS. Nevertheless, as this study
shows, there always remains a small number of
cases who do not have their neurological diseases
correctly diagnosed.
I am greatly indebted to Dr. Kay Hyllested. founder and head
of the Danish MS Register for most kind and valuable assistance.
1. Allison R S. Millar J H D. Prevalence and familiar incidence
of disseminated sclerosis. Ulster Med J 1954 (suppl
2) 235-91.
2. McAlpine D. Course and prognosis. In: McAlpine D,
Lumsden C E. Acheson E D, eds. Multiple sclerosis. A
reappraisal. Edinburgh: Churchill Livingstone, 1972: 197-
3. Kurtzke J F. Diagnosis and differential diagnosis of multiple
sclerosis. Acta Neurol Scand 1970:46:484-492.
4. Lumsden C E. The neuropathology of multiple sclerosis.
In: Vinken P J, Bruyn G W. eds. Handbook of clinical
neurology. Amsterdam: North Holland 1970217-309.
I I .
21 I
Fog T. The topography of plaques in multiple sclerosis.
Acta Neurol Scand 1965:41 (suppl. 15):9-18.
Brownell 8, Hughes J T. The distribution of plaques in the
cerebrum in multiple sclerosis. J Neurol Neurosurg Psychiat
Raine C S. Demyelinating diseases. In: Davis R L. Robertson
D M. eds. Textbook of neuropathology. Baltimore:
Williams & Wilkins. 1985:468-547.
Matthews W B, Acheson E D. Batchelor J R, Weller R D.
In: McAlpine's multiple sclerosis. London: Churchill
Livingstone, 1985: 167-209.
Trojaborg W, Petersen E. Visually and somatory evoked
cortical potentials in multiple sclerosis. J Neurol Psychiatry
Thompson E J, Kaufmann P. Shortman R C, Rudge P,
McDonald W 1. Oligoclonal immunoglobulins and plasmacells
in spinal fluid of patients with multiple sclerosis.
Br Med J 1979:1:16-17.
Perkin G D. Sethi K. Muller B R. IgG ratios and oligoclonal
IgG in multiple sclerosis and other neurological disorders.
J Neurol Sci 1983:60325-336.
Gize R W. Mishkin F. Brain scans in multiple sclerosis.
Radiology 197097:297-299.
Murray S, Veidlinger 0 F. Serial radionucleotide scans in
multiple sclerosis. Can I Neurol Sci 1978:5:321-223.
Cala L A, Mastaglia F L. Computerised axial tomography
in multiple sclerosis. Lancet 1976:1:689.
Gyldensted C. Computer tomography of the brain in multiple
sclerosis. Acta Neurol Scand 1976:53:386-389.
Lukes S A, Crooks L E, Aminoff M J, et al. Nuclear
magnetic resonance imaging in multiple sclerosis. Ann
Neurol 1983592-601.
Jacobs L, Kinkel P R, Kinkel W R. Clinical nuclear
magnetic resonance (NMR) correlations in multiple sclerosis
(MS) abstracted. Neurology 1984:34 (suppl 1):141.
Runge V W, Price A C, Kirshner H S, Allen J H. Partain
C L. James A E. Magnetic resonance imaging of multiple
sclerosis: a study of pulse-technique efficacy. Am J Radio
l984:143: 1015-1029.
Gartner S. Optic neuropathy in multiple sclerosis. Arch
Ophthalmolol 1953:50718-726.
Ulrich J, Groebke-Lorens W. The optic nerve in multiple
sclerosis. Neuroophthalmology 1983:3: 149- 159.
Toussaint D, Pkrier 0, Verstappen A, Bervoets S.
Clinopathological study of the visual pathways, eyes, and
cerebral hemispheres in 32 cases of disseminated sclerosis.
J Clin Neuroophthalmol 1983:3:211-220.
Tine Engell, MD
The Eye Department
Hvidovre Hospital
Kettegards AIM 49
2650 Hvidovre
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PostPosted: Tue Dec 04, 2012 2:13 pm    Post subject: Reply with quote

I found this statement interesting:

Differential diagnosis between MS and other
neurological diseases may occasionally be difficult, especially if the patient is observed over a short period.

I've noticed while reading posts on MS boards how many new patients don't understand that time often has to pass before a doctor can be sure of an MS diagnosis.

With MRIs now, that may not be so true, but it's still a valid point, I think. You have to be observed on one day, then on another day maybe months later, and maybe even several times after that, for a more complete picture of how you're really doing.
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PostPosted: Tue Dec 04, 2012 3:08 pm    Post subject: Reply with quote

I see two areas where there has been an improvement and one where there has been a decline since the previous period.
1) MRI rules out a lot of brain abnormalities compressive lesions and brain tumors
2) They now realize that progressive degenerations cannot be diagnosed clinically. Other diseases can be a lot like PPMS accept that mri and spinal tap are normal.
3) They rely too heavily on MRI these days. What my GP writes on my referral letters is: (presumptive) MS (normal MRI: +ve spinal tap). I have been told that I have clinical evidence of lesions disseminated in space (ataxic nystagmus and optic nerve). And, I really think that the fact that I have quite a number of attacks over the years, and that my vision goes blurry when I get over heated (but, it didn't used to), should be enough for a definite diagnosis. I don't doubt that I could find some neurologist that would give me a definite diagnosis, but I cannot be bothered. But, I think that I am an example of the doctors relying too heavily on MRI (there really doesn't seem to be anything else it could be).
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