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NM Neuropathies PDF

This document discusses the evaluation and diagnosis of peripheral neuropathies. It outlines a 4 step approach: 1) Determine if the neuropathy localizes to a peripheral nerve, 2) Identify the pattern of involvement (length-dependent, symmetric, etc.), 3) Determine what types of nerves are involved (motor, sensory, autonomic), and 4) Establish the timing of involvement (acute, chronic, etc.). Common causes of peripheral neuropathy include diabetes, toxins, infections, autoimmune disorders, and hereditary conditions. Evaluation involves a detailed history, physical exam, and electrodiagnostic testing to characterize the neuropathy and identify potential etiologies.

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0% found this document useful (0 votes)
121 views63 pages

NM Neuropathies PDF

This document discusses the evaluation and diagnosis of peripheral neuropathies. It outlines a 4 step approach: 1) Determine if the neuropathy localizes to a peripheral nerve, 2) Identify the pattern of involvement (length-dependent, symmetric, etc.), 3) Determine what types of nerves are involved (motor, sensory, autonomic), and 4) Establish the timing of involvement (acute, chronic, etc.). Common causes of peripheral neuropathy include diabetes, toxins, infections, autoimmune disorders, and hereditary conditions. Evaluation involves a detailed history, physical exam, and electrodiagnostic testing to characterize the neuropathy and identify potential etiologies.

Uploaded by

dr.b
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
You are on page 1/ 63

Karen Nunez-Wallace, M.D.

November 3rd, 2015


 Step 1: Does it localize to peripheral nerve?
 Know your anatomy!

 Step 2: What is the pattern of involvement?


 Length-dependent, non-length-dependent, symmetric,
asymmetric

 Step 3: What types of nerves are involved?


specification?
 Motor, sensory, large, small, autonomic (sweat, bladder
control, blood pressure, GI symptoms, sexual
dysfunction)

 Step 4: What is the timing of involvement?


 Acute, subacute, chronic, relapsing/remitting
 Mononeuropathy: Characterized by sensory and/or motor
disturbances in the distribution of the affected nerve
 Trauma is the most common cause
 Common neuropathies: carpal tunnel syndrome, Foot drop

 Mononeuritis multiplex (multiple mononeuropathy): Usually


secondary to connective tissue disorders such as polyarteritis
nodosa, SLE, Sjogren's syndrome, RA, sarcoidosis, metabolic
disorders, multifocal motor neuropathy
 Pain may be a significant feature, subacute to acute onset

 Polyneuropathy: Diffuse peripheral nerve disorder not confined


to the distribution of a single nerve or a single limb
 Diabetes most common cause
 Length-dependent, symmetric
 Certain drugs and toxins can affect sensory or motor fibers or both
 Chronic:DM, EtOH, Vitamin Deficiencies,
CIDP (>8 weeks)

 Subacute:Toxins, Vasculitis, Immune


neuropathies, Paraneoplastic, Uremia,
Porphyria, Diabetes

 Acute:AIDP (GBS), Infection (Lyme disease,


Tick paralysis)
 Diabetes Mellitus
 Alcohol
 Nutrition (B12, B6, B1)
 Guillan Barre Syndrome
 Toxins
 Hereditary
 Endocrine
 Renal
 Amyloid
 Porphyria
 Iatrogenic/Infection/Idiopathic (25%)
 Sarcoid
 Tumor/Trauma
 52yrold man with 3 year history of slowly
progressive numbness and weakness.

 Pins
and needles in toes bilaterally followed
by progression to feet and calves.

 Now pins and needles in fingertips without


difficulty holding things but trips when
walking.

 No family history of similar symptoms


 Strength 5/5 throughout except 4+/5 in flexion
and extension of toes.

 Reflexes were absent in ankles and knees, 1+ in


brachioradialis, 2+ biceps and triceps.

 Vibration was absent in toes, diminished in


ankles and shins, intact in knees; light touch,
temperature and pinprick were diminished below
knees and fingertips; proprioception was intact.

 Romberg sign was positive and gait was mildly


wide-based, minimal difficulty with toe, heel
and tandem gait.
 Step 1: Does it localize to peripheral nerve?
 Know your anatomy!

 Step 2: What is the pattern of involvement?


 Length-dependent, non-length-dependent, symmetric,
asymmetric

 Step 3: What types of nerves are involved?


specification?
 Motor, sensory, large, small, autonomic (sweat, bladder
control, blood pressure, GI symptoms, sexual
dysfunction)

 Step 4: What is the timing of involvement?


 Acute, subacute, chronic, relapsing/remitting
 Sensory studies –
 Sural nerve – NR
 Median, ulnar, radial sensory – normal peak latencies,
borderline amplitudes
 Motor studies –
 Normal latencies, low amplitudes (tibial at abductor hallucis
brevis, peroneal recording at extensor digitorum brevis),
normal amplitude at peroneal recording at the tibialis anterior,
conduction velocities in high 30’s (normal 40 m/s)
 H-reflexes –
 No response
 Electromyography –
 No abnormal spontaneous activity
 Long duration, polyphasic units in gastrocnemius, tibialis
anterior with minimally decreased recruitment
 Normal MUAP morphology in vastus lateralis, gluteus medius,
semitendinosus
 Most common cause of Peripheral Neuropathy

 Incidence 54 per 100,000 per year.

 Axonal degeneration of nerve fibers of all sizes.

 Most common type of neuropathic complication


of diabetes: Distal Symmetric Polyneuropathy

 50% of patients with diabetes will develop DSP.

 20% of patients have DSP at time of diagnosis.


 DSP increases risk of ulceration, contributes
to 60% of lower extremity amputations
 Lack of protective sensation, abnormalities
in blood flow, abnormal sweating, poor
wound healing
 Ulceration related to duration and severity of
hyperglycemia
 Painful DSP – presents in early course
 Pain is length dependent
 Deep aching, burning, sharp, cramping
 More severe at night
 EMG/NCS will show axonal neuropathy, with
reduced/absent SNAPs, length-dependent
 Associated with mild motor conduction
slowing
 DSP can predominantly involve small fibers
(EMG/NCS normal)  Sudomotor testing, skin
biopsy
 More than 50% can have at least 1 additional
potential cause of or contributor to the
neuropathy (half discovered through hx
taking, i.e. alcohol; other through labs, i.e.
B12, SPEP, HIV, Sjogren’s).
 Pathophysiology
 Direct axonal injury
 Nitric oxide-mediated microangiopathy
 Oxidative stress
 Accumulation of glycation end products
 Triglyceride levels
 HTN
 Smoking
 Obesity
 Treatment
 Per previous studies, intensive glycemic control
decreases the risk of neuropathy in DM1
 Data for DM2 less convincing, but do support at
least improvement in outcomes
 Other factors (obesity, triglycerides) can also
contribute to severity and outcome
 Metformin use, can decrease B12 levels
 Diabetic autonomic neuropathy
 Cardiac: Orthostasis, arrhythmia; QT
prolongation
 GI: Gastroparesis, early satiety,
diarrhea/constipaton
 GU: Erectile dysfunction, neurogenic bladder
 Skin: Anhidrosis, dry skin, heat intolerance
 Peripheral dysautonomia: Reduced foot sweating,
cool extremities, hair loss, trophic skin changes
 Central: Hypoglycemic unawareness, reduced
hypoxia-induced ventilatory drive
 Acute diabetic neuropathies
 Treatment-Related Neuropathy (“Insulin
Neuritis”)
 Acute painful sensory neuropathy (DM1>DM2)
 Length-dependent, but can be widespread
 Autonomic dysfunction
 Self-limited
 Diabetic Neuropathic Cachexia (DNC)
 Same features as above, but DM2>DM1, tends to be
non-length-dependent, and is associated with severe
weight loss
 Diabetic Lumbosacral Radiculoplexus Neuropathy
(Diabetic Amyotrophy or DLRPN)
 Most common acute neuropathy associated with diabetes
 Abrupt onset of severe unilateral thigh pain
 Followed by progressive atrophy and weakness
 Can spread throughout the limb, then to other limb after
several months
 Weight loss
 Proximal muscles early in course, followed by distal
 Self-limited; but can be left with permanent deficits
 NOT related to glycemic control; autoimmune
 Immunosuppression or modulation may be effective
 CIDP – controversial
 Focal Diabetic neuropathies
 Cranial (1%) – pupil sparing 3rd, others less clear
 Truncal (thoracic) radiculopathy –
 Acute pain in dermatome with abdominal wall muscles
weakness (bulge during Valsalva maneuver)
 Confused with herpes zoster, may be seen with DLRPN
 Gradual improvement and return to baseline
 Compressive mononeuropathies – Median, ulnar,
peroneal
 A 22 year old man presents with patchy
numbness for 1 year. He recently moved from
Nepal 6 months ago. He has no other medical
problems and is not taking any medications.
 On exam, he has normal 5/5 strength except for
4+/5 in left FDI and ADM, 5/5 in APB, and 2+
reflexes.
 He has normal vibration and proprioception, but
decreased pinprick and temperature in extensor
surfaces of legs, and in the left 4th and 5th digits;
normal sensation in palms and soles.
 Two large hypopigmented anesthetic lesions seen
in the trunk.
 EMG/NCS
 Sensory -
 Sural – normal latency, amplitude
 Median – slightly prolonged latency, low amplitude
 Ulnar - NR
 Motor –
 Peroneal and tibial nerves – normal
 Ulnar – prolonged latency, decreased amplitudes
 Median - normal
 Electromyography –
 Spontaneous activity: Fibs and PSW in left FDI and FCU
 Voluntary activity: Increased duration, polyphasic,
increased amplitude units in the left FDI and FCU
 EMG/NCS are consistent with ….

 Patient’s clinical symptoms are consistent


with…
 Left ulnar neuropathy with chronic and
active denervation
 Clinical findings consistent with Hansen’s
disease (Mycobacterium leprae)
 One of the most common causes of
neuropathy in the developing world (Asia,
South America, Africa).
 Transmission is via nasal mucosa and
subsequent hematogenous spread
 Two forms (predominant sensory sx’s):
 Tuberculoid Leprosy:
 Multifocal, circumscribed areas of anesthesia
 Represents robust cell-mediated response to infection
 Lepromatous Leprosy:
 Widespread anesthesia (confluent multifocality)
 Affects cooler areas of skin (pinnae, extensor surfaces)
 Generally represents disease dissemination due to
inadequate cell-mediated response
 Ulnar nerves commonly affected
 Enlarged peripheral nerves

* Acid-fast bacilli in skin smears or biopsy specimens


A 48 y/o man presents with a 1 year history
burning pain toes, soles and dorsum of feet.
 Exam reveals normal strength, absent ankle
jerks, decreased vibration in toes and
pinprick up to ankles.
 He has mild difficulty with tandem gait.
 His labs show normal GTT, B12, SPEP, sed
rate, TSH, Hep panel.
 EMG/NCS – absent sural nerve potentials,
otherwise normal.

* Anything else you want to order?


 Symmetric, distal, predominantly sensory
 Progress in length-dependent manner (glove-
stocking); slowly progressive, may improve
 No significant motor involvement
 Exam reveals sensory loss in all modalities
distally with absent ankle and even patellar
jerks (may be brisk if co-existing HIV CNS
pathology)
 Prevalence 30 to 60% in HIV patients
 Can develop at any time (mean time 9.5 y)
 Stavudine, didanosine, zalcitabine may
contribute
 HIV-associated demyelinating polyneuropathy
 AIDP – may occur at time of seroconversion
 CIDP – more common, patient’s with intact
immune function; treatment immunomodulatory
 Mononeuropathy Multiplex
 Painful stepwise multifocal process in HIV and
CMV
 Milder form in HIV without CMV – thought to be
autoimmune, treatment immunomodulatory
 Autonomic Neuropathy
 Prevalence unknown
A 45 y/o man presents to the ED with a few
days of blurred vision, urinary retention,
progressive weakness and initially started in
feet and now involve proximal leg muscles.
 On exam, he is hyporeflexic, weakness in the
legs, distal> proximal, impaired vibration,
proprioception and decreased rectal tone.
 Eye exam reveals retinitis.
 CSF shows WBC 30 (80% polymorphonuclear
leukocytes, 10% lymphocytes), protein 65
 He has a history of HIV, non-compliant with
medications
 About 50 to 80% of adults have been infected
 Mild febrile illness or asymptomatic
 Immunocompromised patient –
 Mononeuropathy multiplex
 Rapidly progressive
 Axonal degeneration with +/- demyelination
 Cauda equina
 Lower extremity symptoms with sphincter dysfunction
 MRI L-spine may be normal or show enhancement of
roots
 Severe axonal polyradiculopathy
 What is the most common cranial nerve
affected in Varicella-Zoster infection?
 5th 7th
 8th 9th
 Ramsay Hunt syndrome involve which cranial
nerve:
 5th 7th
 8th 9th
 Following VZV infection, there is chronic
latent infection in dorsal root ganglia
 Reactivation occurs in older or
immunocompromised with pruritic rash in
dermatomal distribution (can occur without
rash – zoster sine herpete)
 Thoracic and trigeminal most common
locations
 Other cranial nerves include 7 th, 8th, 9th
 Ramsay Hunt syndrome – lesions in the
external auditory canal with facial palsy
 HSV 1- cranial neuropathies associated with
meningitis or encephalitis
 HSV 2 – Radiculopathy involving lumbar or
sacral roots with paresthesias and weakness
in the lower extremities, urinary retention
 Hepatitis
C virus with cryoglobulinemia is
associated with which presentation:
 A: Sensorimotor polyneuropathy
 B: Mononeuropathy multiplex
 C: Motor neuronopathy
 D: Mononeuropathy
 E: B only
 F: A and B
 G: A, B, and D
 H: All of the above
 Vasculitic,deposition of immune complexes
in vasa nervorum and subsequent nerve
ischemia
 HCV alone not a risk factor for neuropathy
though reports of HCV without
cryoglobulinemia peripheral neuropathy
 Corynebacterium diphtheriae causes URI with
pseudomembrane in the pharynx
 One week after infection, neurological
complications develop
 Bulbar dysfunction

 In 10 % of patients, demyelinating
polyneuropathy with limb and respiratory
weakness (2 weeks to 2 months after
infection)
 Treatment is with antitoxin
 Borrelia burgdorferi, endemic to the
northeastern US
 Neurological symptoms occur within first
month or tow after infection, acute in onset
 Cranial neuropathies and radiculopathies
(similar to those of structural lesion)
 Most associated with lymphocytic meningitis,
pathology in nerve root as it passes through
subarachnoid space
 Brachial and lumbosacral radiculopathy
 Mononeuropathy multiplex
 Diffuse polyneuropathies, axonal
 Chagasdisease is associated with which type
of neuropathy:

 Sensorimotor demyelinating polyneuropathy


 Sensorimotor axonal polyneuropathy
 Autonomic neuropathy
 Sensory neuronopathy
 Autonomic Neuropathy  Mononeuropathy
 Chagas disease Multiplex
 HIV  CMV
 Cranial Neuropathy  HCV w/ cryo
 Lyme disease  HIV (with or w/o CMV)
 Varicella-zoster virus  Leprosy
 Distal Symmetric  Lyme
Polyneuropathy
 Motor Neuronopathy
 Lyme disease
 Hepatitis C w/ cryoglobulinemia
 Poliomyelitis
 HIV  West Nile
 Inflammatory Demyelinating  Radiculopathy
Polyneuropathy  CMV
 Diphtheria  HSV type 2
 HIV  Lyme
 VZV
 Unmyelinated or thinly myelinated nerve
fibers
 EMG/NCS normal

 Symptoms can be evoked or spontaneous,


paroxysmal with or without increased
sensitivity to various stimuli; may be length-
dependent or diffuse
 May have normal exam, look for systemic
findings (diabetic skin changes,
hepatomegaly, Kaposi sarcoma, ulcers, etc.,
dry mouth or skin).
 Fabry disease
 X-linked
 Deficiency of enzyme alpha-galactosidase leading to
storage of globotriaosylceramide
 CNS and peripheral nerve
 Familial amyloidotic polyneuropathy
 Autosomal dominant
 Mutation of transthyretin gene, TTR
 Deposition of amyloid fibrils in nerves and other
organs
 GBS and CIDP
 AIP
 Weakness
 Attacks precipitated by barbiturates, progestins,
AED’s
 Celiac
 Non-length dependent
 Paraneoplastic
 Sensory neuropathies
 EMG/NCS – all sensory nerves with NR; normal motor
nerves; normal electromyography
 Diffuse symptoms, including hearing loss
 Anti-Hu (lung cancer)
 Toxic
 Idiopathic – 50%
 Chronic, slowly progressive length-dependent
 Hereditary
 HSAN I – serine-palmitoyl-CoA transferase
 HSAN IV – profound loss of pain sensaton, MR; TRKA
 HIV

 Diabetes
 HCV

 Alcohol abuse
 Vitamin excess/deficiencies (B12, B1, B6)
 Vasculitic/immune-mediated (c-ANCA, p-
ANCA, anti Ro/La, Sjogren’s)
 Lyme
A 30 year old man presents with 4 weeks of
severe burning pain and numbness in the feet
up to knees and hands up to elbows. His
symptoms progressed to weakness and
became wheelchair dependent due to ataxia.
 On exam, he has significant loss of sensation
in all modalities in all limbs including
abdomen and areflexia. Strength was 5/5
throughout. EMG/NCS showed absent sural,
median, ulnar and radial sensory responses,
normal motor responses.
 Are there any other questions?

 How do you want to work him up?


 Small, large, autonomic fibers
 Acute
 Severe sensory neuronopathy
 Recovery poor due to toxicity to dorsal root
ganglia cell body

 Chronic
 Lower doses
 Diffuse paresthesias
 Autonomic dysfunction
 Recovery good
 Nucleoside analogs
 Small> large; sensory>motor; axonal
 Lamivudine can involve motor nerves
 Serum lactate increased (reduced pyruvate
conversion to Acetyl Coenzyme A)
 Isoniazid
 Inhibits B6 synthesis
 Ethambutol
 Inhibits mitochondria; optic
 Dapsone
 Non-length-dependent, motor neuropathy;
axonal
 Chloramphenicol
 Mild distal sensory
 Nitrofurantoin
 Length-dependent axonal sensorimotor
 Fluroquinolones
 Reversible sensorimotor axonal polyneuropathy
(extended use)
 Metronidazole
 Sensory>motor axonal polyneuropathy
 Large and small fibers
 Associated with increased CSF protein
 Amiodarone
 6% of patients; severe motor symptoms
 Demyelinating (prolonged distal latencies, absent F-
waves, reduced velocities)
 Can have axonal changes as well
 Procainamide
 Demyelinating ONLY
 Increased CSF protein
 Differential in CIDP patients
 Hydralazine
 Sensory, axonal; can prevent with B6
 Perhexiline
 Demyelinating predominantly
 Mitotic spindle inhibitors
 Vinblastine and vincristine – Sensory, motor, axonal,
can involve cranial nerves
 Paclitaxel and docetaxel –Sensory>motor peripheral
neuropathy
 DNA-binding compounds
 “Platins” – Sensory neuronopathy – direct damage to
dorsal root ganglia
 Proteasome inhibitors
 Bortezomib – small>large fiber; GBS/CIDP rare
 Others
 Thalidomide – sensory>motor axonal; but
nonreversible ganglionopathy reported
 Organic gold salts
 Mixed axonal and demyelinating sensorimotor
 Elevated CSF protein; occasional myokymia
 Colchicine
 Sensory axonal; vacuolar myopathy
 Chloroquine
 Myopathy; mixed axonal / demyelinating
 Increased CSF protein
 Tacrolismus
 CNS toxicity; <1% will develop severe
demyelinating neuropathy, can respond to
IVIG/PLEX
 Which
one of the following drugs can cause a
DEMYELINATING polyneuropathy?
 A: Tacrolismus
 B: Amiodarone
 C: Procainamide
 D: A and B
 E: None of the above
 F: All of the above
 Heavy metals
 Lead
 Subacute moderate or high level exposure (inhaling
industrial aerosolized lead)  non-length-dependent
motor axonal neuropathy with minor sensory symptoms
 Chronic exposure  distal symmetric
 Treatment: Chelation with penicillamine
 Arsenic
 Contaminated water supply or exposure to byproducts of
copper and lead smelting
 Axonal sensorimotor; acute or chronic
 “Mees lines”; skin changes
 Treament: 2,3 – dimercapto-1-propanesulfonate (DMPS)
and 2,3-dimercaptosuccinic acid (DMSA)
 Thallium
 Acute – painful sensory neuropathy with normal
strength and reflexes, alopecia
 Chronic – axonal sensorimotor neuropathy
 Mercury
 Found in batteries and fungicides
 Cognitive, behavior changes, ataxia
 Subacute exposure – motor axonal neuropathy
 Chronic exposure – painful axonal sensorimotor
polyneuropathy
 Organophosphates
 Length-dependent sensorimotor axonal
neuropathy, 7 to 10 days after exposure
 Can also develop myelopathy
 Ethylene glycol
 Glycolate, glyoxylate, oxalate
 Oxalate crystals deposition
 Severe axonal sensorimotor polyneuropathy 5 to
20 days later
 Hexacarbons
 N-hexane, n-butyl ketone; present in glues and
solvents
 Sensory>motor>areflexia
 Acute: mixed demyelinating and axonal
 Chronic: Axonal sensory neuropathy
 Ethanol
 Can be directly from ethanol (sensory) or vitamin
deficiencies (sensory/motor); axonal
 Nitrous Oxide
 Myeloneuropathy by inactivation of cobalamin
 Ciguatera toxin
 Microalgae within dinoflagellates (plankton);
Contaminated fish
 Binds voltage-gated sodium channels
 12 to 48 hours  GI symptoms; paresthesias that last
days to months
 20% death from shock
 Demyelinating neuropathy
 Cobalamin (B12)
 Thiamine (B1)
 Dry form : neuropathy predominant  axonal
sensorimotor neuropathy
 Pyridoxine (B6)
 Low level required by body
 Axonal, sensory>>>motor neuropathy
 Alpha Tocopherol (E)
 Cerebellar ataxia
 Large sensory fibers, degeneration of DRG
 Copper
 Zinc toxicity/bariatric surgery
 Myelopathy, lower motor neuronopathy, optic
neuropathy, axonal sensorimotor polyneuropathy
 Which of the following conditions is most
likely to cause a predominantly motor
neuropathy?
 A: HIV infection
 B: B6 toxicity
 C: porphyria
 D: Sjogren Syndrome
A 38 y/o man with AIDS, presents with a 6
week hx of progressing arm weakness. On
exam, he has diffuse weakness, but more
severe in elbow flexion/extension,
diminished reflexes, fairly normal sensation
to all modalities. EMG/NCS shows axonal
neuropathy. Which medication is the culprit?
 A: Fluconazole
 B: Efavirenz
 C: Dapsone
 D: Azithromycin
 Which of the following abnormalities can
occur in patient swho have a neuropathy due
to toxicity from metronidazole or gold?
 A: High level of uric acid in serum
 B: Low level of glucose in CSF
 C: High level of protein in CSF
 D: Low level of copper in serum
 A 30 y/o man with Type 1 DM develops
paresthesias in the toes and has slowly
progressed up to the knees over the past 2 years,
and now affecting fingertips. On exam, 5/5
strength, normal vibration, proprioception,
reflexes. He has reduced pain and temperature
sensation with gradient up to the knees and
slightly reduced in fingers. EMG/NCS are
normal. What is the most likely diagnosis?
 A. Functional etiology
 B. Syringomyelia
 C. Cervical spondylosis
 D. Small fiber neuropathy
 37 y/o woman from West Virginia presents
with pains in her legs and burning in hands,
increasing over the past 3 weeks. She
recently moved to a new development in an
area that was once used as a waste
depository for a nearby glass and
semiconductor factory. On exam, she has
decreased pinprick / light touch in her feet.
How do you treat this condition?
 A. IV hydration
 C. Hemodialysis
 D. Chelation with penicillamine
 E: IM Dimercaprol
 Whichof the following may cause a
predominantly sensory neuropathy?
 A. Arsenic exposure
 B. N-hexane exposure
 C. Dapsone exposure
 D. Pyridoxine intoxication
 E. Nitrofurantoin
 A 58 y/o man presents with several weeks of
progressive genital and perirectal numbness,
urinary retention, progressive bilateral leg
weakness. He has absent reflexes in the legs.
MRI L-spine shows several nerve roots with
enhancement. EMG shows severe axonal
polyradiculoneuoropathy with active denervation
(fibs, psw’s). CD4 count is 30. What do you
order?
 A. CSF HIV-2 antibody
 B. hepatitis panel, including hep C PCR
 C. HTLV – Type 1 antibody
 D. CSF CMV PCR assay
 E. Cryoglobulins assay

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