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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2745_Библиотеки_им_академика_М_И_Перельмана
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mononeuropathy at the elbow and carpal tunnel
syndrome
Phalen/carpal compression—These common
physical examination maneuvers can also be used to
further assess for carpal tunnel syndrome
Straight leg raise—Evaluate for lumbar
radiculopathy, which could be a cause for lower
extremity paresthesia/dysesthesia
Spasticity
A hallmark sign of upper motor neuron damage is spasticity.
This should be evaluated in both limbs of the upper and lower
extremities. The modified Ashworth scale is the gold standard
for spasticity evaluation (see Table 3.5).
Table 3.5
Modified Ashworth Scale
Grade Description
0 No increased muscle tone
1 Slight increase in tone, spastic catch with release present or minimal
resistance at end range of motion (ROM) during flexion and extension
1+ Slight increase in tone, spastic catch with minimal resistance throughout
remainder of movement (less than half of ROM)
2 Further increased muscle tone throughout most ROM, but affected part
easily moves
3 Considerable increase in muscle tone, passive movement difficult
4 Muscle rigid in flexion or extension
Reprinted with permission from Picone MA, Vincent H, Blitz-Shabbir K, West
CY, Akinsanya J. Lower Extremity Signs and Symptoms of Multiple Sclerosis. In:
Positano RG , Borer JS , DiGiovanni CW , Trepal MJ , eds. Systemic Disease
Manifestation in the Foot, Ankle, and Lower Extremity. Philadelphia, PA: Wolters
Kluwer; 2017:284-300. Table 25.3.
Coordination
Dysdiadochokinesia
Assess with rapid alternating movements, including
finger pinching, hand tapping, or foot tapping
Dysmetria
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Finger-to-nose
Heel-to-shin test
Gait
Gait analysis can be an important aspect of an initial
evaluation in a patient with MS. It can reveal signs of ataxia
illustrated through reduced balance and a wide-based gait
pattern. In addition, it can reveal areas of focal muscle
weakness, such as steppage gait seen with ankle dorsiflexor
weakness, Trendelenburg gait seen with hip abductor
weakness, or leg circumduction, which can be seen with hip
flexor weakness. Spasticity can also affect gait patterns as
illustrated by scissoring gait, which can result from adductor
spasticity. However, depending on the area of spasticity, and
presence of concomitant weakness, a wide variety of gait
patterns and compensatory movements can be seen.
Although gait analysis at the initial visit is an important part of
a comprehensive assessment, monitoring gait at subsequent
follow-up appointments can often hold significant prognostic
value and provide patients/physicians with evidence for
disease worsening. Changes in ambulation/use of assistive
device are directly correlated with disease severity, as
illustrated by the Expanded Disability Status Scale (see Figure
3.2) and can be crucial for identifying disease course. Most
commonly, the timed 25-ft walk is used to assess ambulation
speed, whereas the 6-minute walk has been validated to assess
ambulatory stamina. 3 However, recently, the 2-minute walk
test has been shown to have similar prognostic value to the 6minute walking test in assessment of gait stamina. 11 In
addition, the Tinetti gait and balance test can be used to assess
risk for falls within the next year, whereas the Timed Up and
Go test assesses dynamic balance and mobility (see Table 3.6).
Decline in ambulation can be extremely important to identify,
as it can lead to earlier use of assistive device, which can
decrease fall risk and improve patient quality of life.
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FIGURE 3.2 Expanded Disability Status Scale (EDSS).
Reprinted with permission from Picone MA, Vincent H, BlitzShabbir K, West CY, Akinsanya J. Lower Extremity Signs and
Symptoms of Multiple Sclerosis. In: Positano RG , Borer JS ,
DiGiovanni CW , Trepal MJ , eds. Systemic Disease Manifestation
in the Foot, Ankle, and Lower Extremity. Philadelphia, PA: Wolters
Kluwer; 2017:284-300. Figure 25.3. See eBook for color figure.
Table 3.6
High-Yield Tests for Gait Analysis in Multiple Sclerosis
Walking stamina 6′ or 2′ walk test
Walking speed 25-ft walk test
Assessing risk of falls Tinetti Gait and Balance
Generalized balance/mobility Timed Up and Go (TUG)
Major MS Mimics
As illustrated earlier, the clinical symptoms of MS can vary
depending on the individual and the disease phenotype. Proper
diagnosis of MS typically requires other diseases to be ruled
out first. There are many diseases that can present with clinical
symptoms and time courses similar to MS. It is important to be
aware of the broad range of differential diagnosis, their
defining clinical symptoms, and the specific workup that is
needed to rule out that differential. See the tables for a variety
of conditions with both relapsing-remitting (Table 3.7) and
progressive disease courses (Table 3.8), as well as diseases
that can present as DIS but not DIT (Table 3.9), DIT but not
DIS (Table 3.10), and both DIS and DIT (Table 3.11). These
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charts are not comprehensive, but represent some of major
differentials to be aware of and that should be considered with
a comprehensive workup.
Table 3.7
Differential Diagnosis of Multiple Sclerosis With Focus on Selected
Disorders With a Relapsing Remitting Course
Disorder Clinical Features Other Data
Neuromyelitis
optica spectrum
disorder
Optic neuritis, especially
bilateral or with poor visual
recovery; transverse myelitis;
intractable nausea and
vomiting; paroxysmal tonic
spasms
AQP4-IgG; MOG-IgG;
sometimes OCT
Neurosarcoidosis Optic neuropathy and
myelopathy; facial palsy; early
relapse after stopping steroids;
with or without systemic
involvement
Serum ACE
concentration; chest
radiograph, HRCT, lung
function tests; CT/PET
scan; slit-lamp
examination; tissue
biopsy
CNS vasculitis
(primary or
secondary)
Headache; acute CNS
syndromes including
hemiparesis and ataxia; early
cognitive impairment; with or
without systemic involvement
Serum ANCA (systemic
vasculitis); tissue biopsy
at systemic site or brain
biopsy (if possible)
Susac syndrome Encephalopathy, visual loss,
deafness
Fluorescein angiogram
looking for branch retinal
artery occlusions; OCT;
audiometry
CADASIL Migraine, especially with
complex or prolonged aura;
recurrent acute hemiparesis and
other vascular syndromes;
neuropsychiatric disturbance;
dementia
Testing for NOTCH3
gene mutation; skin
biopsy
Connective
tissue disorders
(SLE/Sjögren
syndrome,
scleroderma,
etc.)
Optic neuritis; longitudinally
extensive transverse myelitis;
systemic involvement;
recurrent miscarriage,
thrombosis (antiphospholipid
syndrome)
Serological testing:
ANA, ENA,
antiphospholipid
antibodies; AQP4-IgG
Behçet disease Brainstem syndrome;
myelopathy (rare); oral and
genital ulceration; intraocular
inflammation
Pathergy testing; HLA
typing
CLIPPERS Subacute ataxia, double vision,
and slurred speech; early
relapse after stopping steroids
Brain biopsy
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Disorder Clinical Features Other Data
Leber hereditary
optic neuropathy
Bilateral sequential optic
neuropathies with poor visual
recovery; more common in
men than in women
Genetic testing
Adapted from Brownlee WJ, Hardy TA, Fazekas F, et al. Diagnosis of multiple
sclerosis: progress and challenges. Lancet. 2017;389(10076):1336-1346.
Copyright © 2016 Elsevier. With permission. ACE, angiotensin-converting
enzyme; ANA, antinuclear antibodies; ANCA, antineutrophil cytoplasmic
antibodies; AQP4, aquaporin 4; CADASIL, cerebral autosomal-dominant
arteriopathy with subcortical infarcts and leukoencephalopathy; CLIPPERS,
chronic lymphocytic inflammation with pontine perivascular enhancement
responsive to steroids; CNS, central nervous system; ENA, extractable nuclear
antigen; HRCT, high-resolution computed tomography; MOG, myelin
oligodendrocyte glycoprotein; OCT, optical coherence tomography; SLE,
systemic lupus erythematosus.
Table 3.8
Differential Diagnosis of Multiple Sclerosis With a Focus on Selected
Disorders With a Progressive Course
Disorder Clinical Features Other Data
HTLV1-associated
myelopathy
Progressive myelopathy;
residence or travel to an
endemic area (especially
West Indies or Japan)
CSF HTLV1 antibody
testing
Dural arteriovenous
fistula
Subacute, progressive
myelopathy
Spinal angiography
Nutritional myelopathy
(vitamin B12 or copper
deficiency)
Subacute progressive
myelopathy or
myeloneuropathy; optic
atrophy (severe B12
deficiency); anemia or
pancytopenia
Serum B12,
methylmalonic acid;
serum copper levels,
ceruloplasmin
Primary lateral sclerosis Spastic quadriparesis or
hemiparesis; with or
without bulbar
involvement; with or
without development of
lower motor neuron signs
Electromyography
looking for lower motor
neuron involvement
Leukodystrophies:
adrenomyeloneuropathy;
Krabbe disease;
Alexander disease;
hereditary diffuse
leukoencephalopathy
with axonal spheroids
Progressive myelopathy
(adrenomyeloneuropathy,
Krabbe disease); bulbar
symptoms, ataxia
(Alexander disease);
early cognitive
impairment (hereditary
diffuse
leukoencephalopathy
with axonal spheroids)
Very-long-chain fatty
acids
(adrenomyeloneuropathy);
genetic testing available
for some leukodystrophies
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Disorder Clinical Features Other Data
Hereditary spastic
paraplegia (especially
SPG5)
Slowly progressive
myelopathy (spasticity
greater than weakness)
with or without other
neurologic symptoms
and family history
Genetic testing
Spinocerebellar ataxias Progressive cerebellar
ataxia, with or without
other neurologic
symptoms and family
history
Genetic testing
Adapted from Brownlee WJ, Hardy TA, Fazekas F, et al. Diagnosis of multiple
sclerosis: progress and challenges. Lancet. 2017;389(10076):1336-1346.
Copyright © 2016 Elsevier. With permission. CSF, cerebrospinal fluid.
Table 3.9
Common Etiologies That Can Be Disseminating in Space (DIS) but Not
Disseminating in Time (DIT)
DIS but not DIT
1. Shower of the cerebral emboli
2. Thrombocytopenic purpura
3. CNS vasculitis
4. Mitochondrial encephalopathy
5. Drugs and toxins
6. Acute disseminated encephalomyelitis
7. Progressive multifocal leukoencephalopathy (PML)
8. Mycoplasma encephalopathy
9. Lyme disease
10. Vitamin B12 deficiency
11. Behçet disease
12. Sarcoidosis
13. Paraneoplastic syndromes
14. Periventricular leukomalacia
15. Psychiatric syndromes
CNS, central nervous system. Adapted with permission from Rolak LA, Fleming
JO. The Differential Diagnosis of Multiple Sclerosis. Neurologist. 2007;13(2):57-
72.
Table 3.10
Common Etiologies That Can Be Disseminating in Time (DIT) but Not
Disseminating in Space (DIS)
DIT but not DIS
1. Tumor (brain or spinal cord)
2. Arteriovenous malformation (brain or spinal cord)
3. Familial cavernous hemangiomata
4. Cervical spondylosis
5. Chiari malformation
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DIT but not DIS
6. Foramen magnum lesions
7. Peripheral neuropathy
8. Leber optic atrophy
9. Adult-onset leukodystrophies
10. Migraine
11. Sjögren disease
12. HTLV-1
13. Cerebellar degeneration
14. Syringomyelia
Adapted with permission from Rolak LA, Fleming JO. The
Differential Diagnosis of Multiple Sclerosis. Neurologist.
2007;13(2):57-72.
Table 3.11
Common Etiologies That Can Be Disseminating in Both Time and
Space (DIT & DIS)
DIT & DIS
1. Cerebrovascular disease (including emboli)
2. Familial cavernous hemangiomata
3. CNS lymphoma
4. Subacute myelo-opticoneuropathy (SMON)
5. CNS vasculitis
6. Migratory sensory neuritis
7. Myasthenia gravis
8. Sjögren disease
9. HIV
10. Eale disease
11. Systemic lupus erythromatosus
12. Lyme disease
13. Porphyria
14. Sarcoidosis
15. Anti-phospholipid antibody syndrome
16. Spinocerebellar degeneration
17. Cerebral autosomal-dominant arteriopathy with subcortical infarcts and
lukoencephalopathy (CADASIL)
18. Psychiatric syndromes
19. NMO (aka Devic disease)
Adapted with permission from Rolak LA, Fleming JO. The
Differential Diagnosis of Multiple Sclerosis. Neurologist.
2007;13(2):57-72.
CNS, central nervous system; HIV, human immunodeficiency
virus.
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Diagnostic Workup
If a patient presents with a clinical history and physical
examination in which the list of differential diagnosis includes
MS, it is important for the nonneurologist to have a basic
framework for an effective MS diagnostic workup. Regardless
of whether a referral is made to a neurologist or other medical
specialist, preliminary data collection can be crucial for earlier
diagnosis and targeted medical management. The following is
a brief summary of the diagnostic tests that can be most
effective for ruling out other etiologies and diagnosing MS.
Laboratory Tests
See Table 3.12 for a list of laboratory tests that should be sent
to evaluate for the most important disease mimics of MS.
Although a medical specialist or neurologist may elect for
additional laboratory tests, such as specific genetic testing, the
following list of tests are a good starting point for diagnostic
workup.
Table 3.12
Comprehensive Laboratory Tests—Multiple Sclerosis
HLA B27 SPEP
ANA Rheumatoid factor
ACE Anti SS-A/B
Anti-cardiolipin AB FTA
Anti-DNA DS Anti-thyroid peroxidase AB
Anti-ENA AB Anti-thyroglobulin AB
CH 50 TSH
C3, C4 complement T4
CBC Urinalysis
CMP Vitamin B6
Copper Vitamin B12
Zinc Vitamin D25
ESR Hepatitis screen
Folate JCV AB
Lipid panel Varicella IgG/IgM
Lyme titer Quantiferon TB
Lupus anticoagulant Gad 65
EBV IgG/IgM Celiac panel
SCL 70 NMO AB
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AB, antibody; ACE, angiotensin-converting enzyme; ANA,
antinuclear antibodies; CBC, complete blood count; CMP,
comprehensive metabolic panel; DS, double strand; ESR,
erythrocyte sedimentation rate; FTA, fluorescent treponema
antigen; JCV, John Cunningham virus; NMO, neuromyelitis
optica; SCL, scleroderma 70; SPEP, serum protein
electrophoresis; TB, tuberculosis; TSH, thyroid stimulating
hormone.
Imaging
MRI continues to be the gold standard for supporting a
diagnosis of MS, as well as searching for other possible
radiological features to support another diagnosis. A
standardized protocol for MRI in MS diagnosis has been
created by MAGNIMS and the Consortium of Multiple
Sclerosis Centers. 12 In short, the panel recommended that a
brain MRI be obtained in all patients being considered for a
diagnosis of MS. In addition, it was agreed upon that, although
spinal MRI is not necessary in all cases, it is advised in the
following cases: spinal cord localization, when there is a
primary progressive course, when considering MS in less
common populations (e.g., older individuals or nonwhite
populations), or when additional data are needed to increase
diagnostic confidence. 13 The specifics of MRI with MS will
be discussed at length in the MRI chapter of this book.
CSF Analysis
A lumbar puncture with CSF analysis assessing for oligoclonal
IgG bands has long been a mainstay in the diagnosis of MS.
However, in recent years, less emphasis has been placed on
using CSF findings for diagnostic purposes, and this analysis
is no longer considered a mandatory clinical test in the setting
of diagnostic MRI findings. That being said, CSF analysis
does have a key prognostic value and role in clinical decision
making. 14 Although the presence of oligoclonal bands in CSF
can be a confirmatory test for MS, it is not specific for MS and
can be found in a variety of other diseases of the CSF. In
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addition, the absence of CSF findings does not completely rule
out an MS diagnosis, because CSF oligoclonal bands may be
absent in individuals early in the disease process and in young
children. 14 However, there continues to be diagnostic utility
with the oligoclonal CSF test. The use of CSF testing for MS
diagnosis is summarized in Table 3.1, in the revised 2017
McDonald criteria.
Electromyography
An electrodiagnostic evaluation can be an important part of the
workup for MS. Although it is not highly specific for MS or
essential to satisfy the diagnostic criteria, it can help to rule
out other etiology that could explain the patient’s symptoms. It
can be helpful for diagnosing peripheral neuropathies, nerve
entrapments such as carpal tunnel, or radiculopathies that
could explain a patient’s symptoms. One should consider
referring a patient for electrodiagnostic evaluation if the
clinical symptoms warrant such workup.
Evoked Potential
This diagnostic test measures electrical activity in the brain
through stimulation of specific sensory nerve pathways. The
test has been shown to detect decreased conduction velocity
along the sensory pathways, which represents evidence of
demyelination in the CNS pathways. In theory, any sensory
pathway can be assessed, but typically visual EPs, short
latency somatosensory EPs, and brainstem auditory EPs are
tested most frequently. Evoked potential (EP) testing can
detect changes in sensory pathway conduction for a variety of
conditions besides MS, including optic neuropathies,
myoclonus, and a variety of other CNS tumors and isolated
brainstem lesions. It is often frequently used for intraoperative
neurologic monitoring during spine surgery. 15 Previously, EP
tests were used to establish dissemination in space by
identifying different locations of CNS lesions in clinical cases
with little or no changes clinically. However, recently, EP has
been removed from the 2017 McDonald criteria, because of its
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