NM Neuropathies PDF
NM Neuropathies PDF
Pins
and needles in toes bilaterally followed
by progression to feet and calves.
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:
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?
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