Peripheral Neuropathy Neurology
Peripheral Neuropathies
• Disorders of the peripheral nerves
• Prevalence 2,400/100,000 (2.5%)
• Increases with age: 8,000 per 100,000 (8%)
• Common
• Symptoms depends on the type of nerves affected
and where the nerve is located in the body
• Neuropathy is a general term referring to disorders of
peripheral nerves. It is common, often distressing and
sometimes disabling
• Peripheral neuropathy can be associated with poor
nutrition, a number of diseases, nerve compression,
exposure to toxins or inflammation
• One or more types of nerve may be damaged
• Prognosis of neuropathy depends on the underlying
cause. The earlier the diagnosis is made and
treatment is started, the greater the chance that nerve
damage can be slowed or reversed and the better the
prognosis
Pathogenic Mechanism
1. Secondary degeneration of the axons and myelin
sheaths
2. Alteration of the function and structure of the ventral
and dorsal column of the spinal cord
3. A pathologic process in the CSF or leptomeninges
may damage the exposed spinal roots
4. Diffuse or localized arterial diseases may injure
nerves by occluding their nutrient arteries
a) vaso nervorum  blood supply of the nerves
can be injured
5. Cellular or humoral attack on various components of
myelin
6. Toxic or immunologic agents that selectively damage
the Schwann cells or their membranes, cause
demyelination of peripheral nerves leaving axons
relatively intact
*Secondary cause of degeneration are less severe compared
to primary causes
Pathologic Reactions
• The myelin sheath – most susceptible element of the
nerve fiver
o Why susceptible? It may break down as a
part of a primary process involving schwann
cells or the myelin sheath itself, or it may be
damaged secondarily as a consequence of
disease affecting its axon
o Nodes of Ranvier: gaps between myelin
sheath with high concentration of sodium
channels  salutatory electrical conduction
• Focal degeneration of the myelin sheath with sparing
of the axon is called segmental demyelination
(example: GBS)
o Secondary demyelination  myelin
degeneration after a primary axonal disease
• Myelin may also degenerate secondary to axonal
disease
o Process that may occur either proximal or
distal to the site of axonal interruption
• Wallerian Degeneration – “dying forward”. A
process in which the nerve degenerate from the point
of axonal damage outward
o Dying forward usually secondary to trauma
• When the axon degenerate as a part of a “dying
back” phenomenon in a more generalized
metabolically determined polyneuropathy, it is termed
axonal degeneration (example: Diabetic)
o Toxic metabolic secondary to drug
intoxication (overdose of dapsone, INH) can
lead to dying back mechanism
o The “lightning bolts” indicate that the toxin is
acting in multiple sites along the sensory and
motor axons of the central and peripheral
nervous systems. By the late stage, axon
degenerating has moved proximally (dying
back). CNS recovery is impeded by astroglial
proliferation
• Destruction of an anterior horn cell or proximal
motor root results in a gradual dissolution of the
distal motor nerve and its myelin sheath (a form of
Wallerian degeneration)
• Certain disease affect the neuron primarily rather than
the axon and cause either motor or sensory
neuronopathy
o Attack of mainly the mother cell in contrast to
neuropathy
o Can either attack the anterior horn cell
(motor neuronopathy such as poliomyelitis)
or the dorsal root ganglion (sensory
neuronopathy)
• Central ganglion neuropathy: Proximal: face, hand
• Diabetic neuropathy: start most distal at feet and
progressively goes up
Teased Fibers: Segmental Demyelination (above picture)
• Usually only a short segment has an absence of
myelin to the account for saltatory condunction
• However in segmental demyelination, there is a
greater absense of myelin and normal saltatory
conduction of the nerves becomes impaired and rate
of neuronal transmission is slowed
3 physiological properties of demyelination
1. Delay in latency
 Normal: 4 miliseconds
 Demyelination: 6-8 miliseconds

2. Slowing of conduction velocity
3. Conduction block
(+) Myelin Ovoids
 Characteristic of
a axonal
degeneration
than segmental
degeneration
Nerve Conduction Studies
Conduction block makes you weak (akala mo smile ko lang
makes you weak pati pala conduction block)
Advantages of EMG/NCV
• Determine if a nerve injury is present
• Localize the site of injury along the course of the
motor unit
• Suggest nerve pathology (axonal or demyelinating)
• Prognosis
Symptomatology
Impairment of Motor Function
• Polyneuropathies are generally marked by a
symmetric distribution of the weakness or paralysis
• In cases of diffuse axonal damage, the muscles of the
feet and legs are affected earlier and more severely
than those of the hands and forearms
• “length dependent” pattern of axonal degeneration
• Distal axonal pattern in nutritional, metabolic and toxic
neuropathies
o Distal pattern not generally found in acute
and chronic demyelinating inflammatory
neuropathies
• Paraparesis is NOT TYPICAL of the generalized
neuropathies but can be observed in infection and
inflammation of cauda equina
Sensory Loss
• In toxic and metabolic neuropathies, sensory loss
exceeds weakness; and in sensory neuronopathy,
there is no motor deficit
• In the polyneuropathies, sensation is affected
symmetrically in the distal limbs and more in the legs
than arms
• All sensory modalities (touch-pressure, pain and
temperature, vibratory and joint position senses) are
impaired or eventually lost, although one modality
may be affected out of proportion to the other
• Vibratory sense is often affected more than position
and tactile senses
• Sensory nerve damage can produce tingling,
numbness or pain
• Universal sensory loss  attributed to acquired
disease affecting sensory ganglia seen in
paraneoplastic process
Peripheral Neuropathy Neurology
Tendon Reflexes
• The rule is that diminution or loss of tendon reflexes
is invariably a sign of peripheral nerve disease
• In neuropathies that affect the largest diameter,
heavily myelinated fibers, the tendon reflexes are
diminished early and out of proportion to weakness
• Loss of sensory functions that are dependent on the
large fibers in the presence of preserved reflexes
implicates that central projections of the sensory
ganglion cells
• Note: A patient may or may not present with sensory
loss but diminution or absence of DTR (especially if
asymmetric)  will always tell you that this is
neuropathy rather than muscle disease or myoneural
junction disease
Paresthesias, Pain and Dysesthesias
• Certain neuropathies cause pain which may be
described as burning, aching, sharp and cutting or
crushing and at times may resemble the lightning
pains of tabes dorsalis
• Perversion of sensation (allodynia) is common place
o Allodynia – perception of a nonpainful
stimuli as painful (akala mo di masakit pero
masakit pala  may feelings na pala ayun
GG)
• The sensory threshold is actually raised and it is the
sensory experience or response that is exaggerated
(hyperpathia)
o Hyperpathia – exaggerated response to
painful stimuli (Di naman kayo nasaktan ka
naman, ano ba)
• Painful paresthesias and dysesthesias are particularly
common in certain types of diabetic, alcoholic-
nutritional, and amyloid neuropathies
o Alcohol neuropathies according to dr. is not
really true, it may be caused bu malnutrition
combined with excessive alcohol intake. Not
seen in PH because we have pulutan unlike
in western countries.
• A particularly intense form of burning pain typifies the
causalgia of a partial nerve lesion (usually traumatic)
of the ulnar, median, posterior tibial, peroneal, or
occasionally some other nerve
• Treatment modalities will differ for patient with (+)
neuropathic pain and in (-) neuropathic pain
o Pregabalin, gabapentin are supposed to be
given for positive symptoms of neuropathic
pain (burning, pins and needles and NOT for
numbness)
Sensory Ataxia and Tremor
• Involvement of dorsal column in spinal cord
• Proprioceptive deafferentation with retention of a
reasonable degree of motor function
• In the chronic sensory neuropathies with ataxic
features, all movements, though strong, are rendered
ineffective by virtue of the deep sensory loss
• Also seen in Tabes Dorsalis
o Ataxia without weakness
o Occurs secondary to neurosyphilis
o Increased in patient with HIV/Aids
 Peripheral Neuropathy Neurology

Autonomic Dysfunction
• Anhidrosis Clinical Forms of Neuropathy
• Orthostatic Hypotension • Polyneuropathy
o Two of the most frequent manifestation • Radiculopathy
• Small or medium sized unreactive pupils • Neuronopathy (motor/sensory)
o Unusually sensitive to other drugs • Mononeuropathy
• Lack of sweat, tears, and saliva • Multiple mononeuropathies
• Sexual impotence • Plexopathy
o Consider either diabetic autonomic
neuropathy or depression Polyneuropathy
• Weak bowel and bladder sphincters with urinary • Generalized process affecting the peripheral nerves
retention or overflow incontinence • Weakness is symmetrical and progress bilaterally
• Weakness and dilatation of the esophagus and colon • Reflexes are lost
o Slowing of GI motility (Gastroparesis, IBS or • Sensory complaints are more pronounced distally
constipation • Starts at Lower extremities
• Vagal and other parasympathetic dysfunction – • “Symmetrical and Diffuse”
normal variability of heart rate with respiration (sinus
arrhythmia) is lost, paralytic ileus or dyscoordinated Polyradiculopathy
peristalsis, achlorhydria and hyponatremia • Affects multiple spinal roots
• In general these autonomic disturbances corresponds • Neurologic signs are symmetrical with an erratic
to degeneration of unmyelinated fibers in the distribution
peripheral nerves • Pain in the sensory distribution of the roots called
o Some patient have (-) EMG/NCV  doesn’t radiculopathy
mean patient don’t have neuropathy, small • Limitation of sensory loss to one of the dermatomes
fibers might be affected and
o EMG/NCV  (+) in large fibers onlu Neuronopathy
• Affects the ganglion cells
Fasciculations, Cramps and Spasms • Sensory neuronopathy – loss in both proximal and
• All the affected muscles ripples and quiver and distal distributions
occasionally cramp • Motor neuronopathy – disorder of the anterior horn
o Patient may be prescribed Schwepps Tonic cells causing weakness, fasciculations and atrophy in
Water which contains small amounts of a widespread distribution
quinine (anti-malarial drug) that may aid in
relief of cramps Mononeuropathy
 Decreases excitability of motor end • Weakness and sensory loss in the territory of a single
plate  decreasing muscle peripheral nerve
contractility • Local cause
 Use with caution: Patient with renal • Direct trauma, compression, entrapment
failure and should be avoided in
patient with liver disease Ulnar Ulnar groove, cubital tunnel
Median Carpal Tunnel
Approach to the Patient with Peripheral Neuropathy Peroneal Fibular head
• The examiner determines: Tibial Tarsal Tunnel
o Tempo/Progression  Multiple mononeuropathy
o Distribution o Cumulation of multiple
o Severity mononeuropathies, mononeuritis multiplex,
• Key Points in the Evaluation of Peripheral Neuropathy may at times be difficult to differentiate from
o Progression polyneuropathy
 Smoothly Progressive: DM o Vasculitis should be the differential when
 Stepwise: Secondary to vascular or patient presents with multiple
connective tissue disease mononeuropathies
 Relapsing/Remitting: Chronic
Inflammatory Demyelinating Plexopathies
polyneuropathy and MS • Only one limb is affected but the motor, sensory,
o Which fiber are involved and the reflex loss do not conform the pattern of
 Motor: Guillain-Barre Syndrome several adjacent nerve roots or nerves
 Sensory: • Multiple nerve distribution in one limb but they aren’t
 Large fibers: sensory all grouped together, they are not coordinated
ataxia • Example: Klumpkes or erbs
 Small fibers: Neuropathic
pain Important Historical Data
 Autonomic • The pattern of neuropathy sets limits on the etiologic
GBS is a motor neuropathy possibilities
Diabetic generally sensory but also motor
 Peripheral Neuropathy Neurology

• Determine whether the process is predominantly • Weakness that evolves more or less symmetrically
motor with less sensory involvement or the converse over period of several days to a weeks
• An acute onset with rapid evolution is nearly always • Involves both proximal and distal
diagnostic of an inflammatory, immunologic, toxic, or • Usually lower extremities before upper
vascular etiology + Trauma and entrapment • In 5% of cases there is total motor paralysis with
• A polyneuropathy evolving slowly over many years, respiratory failure within a few days
is indicative of a hereditary or a metabolic disease
o Hereditary: Demyelination is uniform History of illness
(Charcot-Marie-Tooth) • Pain and aching discomfort in the muscles of the hips,
o Acquired: Different grades thighs and back
 One limb grade 20, other limb • Sensory loss may occur during the first days of illness
grade 40. • Reduction of vibration and position sense
• Muscle atrophy signifies a process of relatively long
standing etiology Physical Findings
• Absent tendon reflex (Areflexia)
Ancillary Procedures o Most important physical findings
• EMG-NCV o Sabi ni doc sa early days daw meron pa
• Biochemical test (metabolic, nutritional, or toxic) pero habang tumatagal nawawala na yung
o Metabolic: Thyroid, DM reflex, parang feelings mo lang.
o Nutritional: Vit B12 • Arm muscle are less weak
o Toxic: Lead, Mercury (Gold panning, • Facial diplegia in 50%
Minamata disease) • Autonomic disturbances (sinus tachycardia, facial
• CSF examination flushing, fluctuating hypertension and hypotension,
o Cytoalbuminous dissociation (elevated loss of sweating, episodic diaphoresis)
proteins, normal cells) • Urinary retention in 15%
 Most common in GBS
 When myelin is destroyed  GBS Variants
protein is released  Regional
 GBS  high protein release and o Fisher Syndrome/Miller Fischer
may present with increased ICP Syndrome (lalabas daw to!)
because of too much destruction  Opthalmoplegia
• Nerve and muscle biopsy  Ataxia
o Vasculitis or Polyartheritis nodosa  Areflexia
• Measurement of immunoglobulins and antineural o Cervicoo-brachial-pharyngeal
antibodies o Oculopharygeal weakness
o Helpful in paraneoplastic conditions o Predominant paraparesis
o Neuropathies precede malignancies o Bilateral facial or abducens weakness with
• Genetic testing distal paresthesias
o Ophthalmoplegia with GQ1b
Acute motor paralysis with variable disturbance of autoantibodies
sensory and autonomic function • Functional
• Acute inflammatory demyelinating polyneuropathy o Generalized ataxia without dysarthria or
• Vasculitic Polyneuropathies nystagmus
• Porphyria o Pure sensory
• Toxic Polyneuropathies o Pure motor
• Acute sensory and autonomic polyneuropathies o Pandysautonomia
o Axonal
Guillain-Barre Syndrome (AIDP)
• AIDP – Acquired Immune demyelinating Laboratory Findings
polyneuropathy • Electrodiagnostic studies
• Most common cause of acute or substance o Reduction in the amplitude of muscle action
generalized paralysis potentials, slowed conduction velocity, and
• Occurs in all parts of the world in all seasons conduction block in motor nerves
• Affecting children and adults of all ages and both o Prolonged distal latencies and absent F-
sexes responses
• Usually preceded by mild respiratory or o H reflex is almost always very delayed
gastrointestinal infection • CSF examination
• Latest possible cause: Zika Virus; previously: o Normal pressure
Campylobacter o Acellular or contains only a few lymphocytes
o Increase in CSF protein reflects the
Symptomatology inflammatory process of the nerve roots
• Parasthesias and slight numbness in the toes and (cytoalbuminous dissociation)
fingers
Pathologic Findings
 Peripheral Neuropathy Neurology

• Perivascular (perivenous) lymphocytic infiltrates o Hypertrophy: cases of long duration

• Segmental demyelination and a variable degree of o Gadolinium enhancement
Wallerian degeneration  Active disease
• The cellular infiltrates are scattered throughout the  Very common in children
cranial nerves, ventral and dorsal root ganglia and
along the entire length of peripheral nerves
Associated Disorders
Pathogenesis and Etiology • Monoclonal antibodies (M-protein)
• Cell-mediated immunologic reaction directed at o IgG and IgA
peripheral nerves o Rarely IgM
• HIV
Differential Diagnosis • Diabetes
• Acute spinal cord disease • Other possible associations:
o In acute spinal cord  (+) sensory level, so o Chronic active hepatitis
not a peripheral disease o GVHD
• Poliomyelitis o Nephrotic syndrome
o Recently, mono because of advent of oral o CNS demyelination
polio vaccines o Lymphoma
o In the past patients presented with quadri o Interferon a treament

Treatment Treatment
• Admission • Try individual therapies sequentially
• Respiratory assistance and careful nursing • Response to one does not predict efficacy of others
• IVIG 0.4g/kg/day x 5 days • Therapeutic Modalities
• Plasmapheresis – 4-6 treatments o Prednisone: 60 to 100 mg/day PO then taper
• Reduces by half hospitalization days  Start tape after: 3-6 months or
Note: 2 treatments for AIDP clinical improvement begins
 IVIG  Taper slowly
 Plasma pheresis  Initially 5mg on alternative
 DOES NOT respond to steroid unlike CIDP days q2 to 4 weeks until
80mg and 10 mg
Chronic Inflammatory Demyelinating Polyneuropathy  Then 2.5 mg on alternative
• CIDP days q2 weeks to 80 mg
• Time course: Variable types and 0mg
• Chronic Progressive: 60%  Then taper high day dose
o Months (>2) to years by 5 mg q4 weeks until 40
o Often reach plateau mg and 0 mg
o Onset age: Older, Mean 51 years  Then by 2.5 mg q4 weeks
• Relapsing: 30%  Minimum dosage is qod if
o Onset Age: younger, Mean 27 years possible
• Acute onset: 15%  Many CIDP patients will relapse if
o Weeks to 2 months prednisone is stopped without
• Monophasic with remission: especially children additional immunosuppression
• Prognosis worse with o Methyprednisone (IV): 1g/day x 5
o Progressive course  Then intermittent tapering additional
o CNS invlolvement iv or oral doses (1gram): weekly to
• Pathology: More axonal loss monthly
o Human Immune Globulin
Electrophysiology  1g/kg/day x 2: repeat q3 to 8 weeks
• Conduction block  400mg/kg 1 to 2x per week for 8 or
• Slow nerve conduction velocities more weeks
o <80% of lower limit of normal o Cyclosporine A
o Variable velocities among nerves  Initial treatment when prednisone
 DDx: HNPP and CMTX not indicated
o Motor and sensory  Dose: 2.5mg/kg bid then taper to
• CMAP changes minimum effective dose
o Temporal dispersion o Plasma exchange
o Prolonged distal latencies o Azathioprine
• F-waves  To lower corticosteroid or
• Amplitude of sensory potentials cyclosporine dosage
 Dose: 2.5 to 3 mg/kg
MRI o Methotrexate: 7.5 to 25 mg po on weekends
• Abnormal CNS in 5%
• Spinal roots and plexus
 Peripheral Neuropathy Neurology

o Clyclophosphamide: monthly IV pulse x 6;

for refractory patient

Anatomic classification of Peripheral Neuropathy

• Mononeuropathy (Focal neuropathy)
• Mononeuropathy Multiplex (multifocal neuropathies)
o DDX: VASCULITIS!!
• Polyneuropathies (Symmetrical, Generalized)

Disorder of Peripheral Nerves

• Genetically determined polyneuropathies
o Charcot-Marie-Tooth (CMT) syndromes
 CMT1: hypertrophic demyelinating
 CMT2: neuronal
 CMT3: Infantile onset; Dejerine-
Sottas
 Other CMT syndromes
o Hereditary sensory and autonomic
neuropathies
o Hereditary neuropathies with known
biochemical abnormalities
 Familial amyloid polyneuropathies
 Porphyria
 Metachromatic leukodystrophy
 Refsum’s disease
 Lipoprotein deficiencies
 Others

• Acquired polyneuropathies
o Guillain-Barre syndrome and related
disorders
 Acute demyelinating or axonal
polyneuropathy
 Chronic Relapsing demyelinating
polyneuropathy
 Miller-Fischer Syndrome
o Polyneuropathy with paraproteinaemia or
dysproteneinaemia
 Multiple myeloma
 Benign monoclonal gammopathy
 Macroglobulinaemia and
Cryoblinamia

Pathogenesis

Stage 1: Lymphocytes migrate through endoneural vesselss

and surround nerve fiver, but myelin sheath and axon not yet
damaged
 Peripheral Neuropathy Neurology

o Polyneuropathy with malignant disease

 Paraneoplastic neuropathies
 Infiltrative polyneuropathy
o Polyneuropathy with connective tissue
disease
o Polyneuropathy with infection
 Leprosy
Stage 2: More lymphocytes extruded and macrophages  Herpes zoster
appera. Segmental demyelination begins; however, axon not  HIV
yet affected. Typically early
pattern of sensory
loss in leprosy
(hansen’s disease)
tends to affect
cooler skin areas,
not following either
segmental or nerve
Stage 3: Multifocal myelin sheath and axonal damage. Central distribution. Area
chromatolysis or nerve cell body occurs and mucle begins to kept warm by
develop denervation atrophy. watchband not
affected.

Moderate skin lesion

of face and ears

Skin lesions. Central

healed are tend to
be hypesthenic or
Stage 4: Extensive axonal destruction. Some nerve cell anesthetic
bodies irreversibly damaged but function may be preserved (dimorphorous
because of adjancent less-affected nerve fibers leprosy)
Conduction Block Painful
Distal Stimulation Proximal Stimulation erythematous
• Large CMAP • Reduced CMAP size vesicular eruption in
to <50% distribution of
• Reduction occurs ophthalmic division
focally along nerve of R trigeminal
Conduction block results in weakness even if EMG/NCV nerve
results have not changed. Remyelination will take longer than
the reversal of the conduction block and thus may not be
evident yet on EMG/NCV.

Watch out for weakeness of diaphragm and other respi

muscles  early detection and correction  Give treatment
(NOT steroids BUT IVIG and plasmaphresis)

o Metabolic Polyneuropathies
 Nutritional neuropathy
 Alcoholic neuropathy
 Diabetic neuropathy
 Favorite nerve: CN3 , CN6
least in facial
 Uraemic neuropathy
 CKD: restless leg
syndrome is indicative but
not pathognomonic
 Hepatic neuropathy

 Others
o Toxic Polyneuropathies
 Diphtheria
 Heavy metal poisoning
 History of nausea and
vomiting  suggest
arsenic poisoning in
patient with
polyneuropathy
 Rat poison: most readily
available source of arsenic
 Other source: antique
copper untensils and
runoff waste from copper
smelting plant.
 (+) Mees Lines in Nails in
arsenic poisoning
 Lead poisoning: Request
for peripheral smear
(Basophilic stippling of
RBC)  then request for
24 hr. urinalysis
 Organic solvent toxicity
 Drug toxicity
 INH, Disulfiram,
Vincristine, Hydralazine
• Mononeuropathies
o Physical injury
 Trauma
 Compression
 Radiation
 Ischemic and vasculitic
 Hemorrhage
o Tumors arising in nerve
Most common mononeuropathhies
Facial Mononeuropathy
that affects cranial nerves
(Bell’s Palsy CN7)
Cause: Idiopathic
Most common chronic entrapment
peripheral neuropathy
Median Mononeuropathy
(Carpal Tunnel Syndrome) Thenar atrophy and waking up due
to tingling and pain in thumb,
index, middle finger
Other compressive or entrapment neuropathies
Compression of nerve on hard
surface
Ulnar Nerve
Numbness and tingling distribution
in hand and interosseous wasting
between thumb and index finger
Compression of nerve in axilla or
upper arm in patient sleeping with
arm over chair back, edge of bed or
Radial Nerve
using crutches.
Wrist Drop (Saturday Night Palsy)
Compression of common peroneal
nerve over fibular head by cast. In
debilitated patient sitting with legs
Peroneal Nerve
crossed or inebriate sleeping on
side of hard surface
Peripheral Neuropathy Neurology
Foot Drop
Entrapment of nerve under inguinal
ligament
Lateral Femoral Cutaneous
Nerve Meralgia Paresthetica  pain on
lateral side of thigh (people wearing
corset)
Diabetic Neuropathy
• Most common polyneuropathy
• May be focal, multifocal, or diffuse symmetrical
• Some cases seen before onset of chemical diabetes
– IGT neuropathy
o Does not meet criteria but has sign and
symptoms
o Reversible: Lifestyle change
• Most common in >50 years of age
• FBS 126mg/dl  Retinopathy was first seen
Clinical Syndromes
• Distal, symmetrical, sensory polyneuropathy
• Acute ophthalmoplegia (CN 3 or 6)
• Acute mononeutopathy of limbs and trunk
• Diabetic amyotrophy
• Symmetrical proximal motor weakness and wasting
• Autonomic neuropathy
• Painful thoracoabdominal radiculopathy
Pathology and Pathophysiology
• Demyelinative
• Axonal Degeneration
• Combined
• Vascular-ischemic
• Biochemical – myoinositol, polyol pathway
• Trophic factiors (NGF, VEGF, etc)
Treatment
• Preventive treatment – maintain blood glucose close
to normal range
• Aldose reductase inhibhitors
• Gangliosides
• Gene therapy (VEGF)
• NGF Injections
• Pain Treatment – amitriptyline, SSRIs, Gabapentin,
Pregabalin
• Diabetic patient taking metformin interfere with
vitamin B complex absorption  only time you give
Vit B in Diabetic patient
Disorder of Motor Nerve Roots
• Physical Compression of nerve roots
o Disc prolapse
o Bony compression
o Tumor
o Trauma
• Radiation
• Infective and post-infective
• Immunologically mediated radiculopathies
• Neoplastic infiltration
Cervical Disc Herniation (+) Spurling’s Manuever
 Peripheral Neuropathy Neurology

Peripheral
Neurofibromatosis
Dumbbell tumor of spinal
nerve root

Plexus Lesion (not discussed)

Parsonage-Turner Syndrome
 Other names: Brachial neuritis, Brachial Plexitis,
Neuralgic Amyotrophy
 Develops abruptly in an otherwise healthy individual;
it may also complicate an infection, injection of
vaccine or antibiotic, childbirth, surgical procedures or
any type and use of heroin
 Clinical and EMG findings suggest a lesion of the
peripheral nerves of the shoulder girdle and upper
arm rather than in cords of plexus
 Male>Female
 Ages 20-65 (adults)

Signs and Symptoms

 Ache or deep burning in and around the shoulder
centered over deltoid, root of the neck or in the axilla
o Pain becomes rapidly very intense
o Abrupt and awakens the patient to sleep
o Aggravated by movement of muscles
Lumbar Disc Herniation involved
o Narcotics for pain relief
o After several days: Muscle weakness
develops causing sensory and reflex
impairment
o Pain subsides as muscle weakness
appears
o Most cases are unilateral, but small portion
of cases are bilateral in outset
 Complete paralysis of either serratus anterior,
deltoid, biceps or triceps (total or in isolation)
 Most neurological deficit have been localized in
around shoulder and upper arm
 Either Biceps or Triceps reflex may be abolished
 Few cases: additional of median, radial, anterior or
posterior interosseous nerve palsy detected by EMG
 No fever, leukocytosis or increased sedimentation
rate
 Occasional mild pleocytosis, slight increased protein
in CSF, but most cases have normal formula and
sampling of CSF is not necessary for diagnosis
 Recovery of paralysis and restoration of sensation are
complete in 6-12 weeks, but sometimes not for a year
or longer
 Residual weakness and wasting of affected muscles
and some have recurrence on the same or opposite
side
 Motor nerve conduction becomes impaired in 7-10
days
o The most common: Serratus anterior palsy
(long thoracic nerve)
 Peripheral Neuropathy Neurology

o Other nerves occasionally affected:  Usually due to anticoagulants  lumbosacral plexus

surprascapular, axillary, posterior
interosseous, and phrenic nerves
 If phrenic is affected: mild dyspnea
on exertion and one hemi
diaphragm is elevated on CXR
 This syndrome can follow parvovirus B19 infection
o most cases had been preceded within days
by an erythematous rash spreading from
limbs to trunk and face (somewhat similar to
eruption of fifths disease)
o Some have influenza like symptoms and
adenopathy
 Typical brachial neuritis can also occur as part of
febrile illness caused by CMV infection and in
patients with AIDS
 Cozsackievirus was suggested to be a possible
cause of brachial neuritis
 Today, rare disease because of injection of tetanus
toxoid, typhoid-paratyphoid vaccine and DTP
 Plexitis also occur as an uncommon idiopathic
complication of postpartum state.
 One must differentiate idiopathic brachial plexitis from
the following condition
o Spondylosis or ruptured disc with root
compression particularly C5 and C6 roots
o Brachialgia from bursitis, labral tear or
rotator cuff syndrome
o Polymyalgia rheumatica
o Entrapment neuropathies, particularly
subscapular or dorsal scapular nerve
o Carcinomatous plexopathy
o Radiation plexopathy
o Sarcoid and other granulomatous
infiltrations.
 Pathologic data: mononuclear inflammation in
fascicles of plexus obtained by bioplsy
 Presence of Perivascular lymphocytes at endoneural
space and less in epineurium
 Treatment
o Symptomatic
o Steroids and immunosuppressant

Other Plexus Lesions

Secondary to Birth Trauma
Upper Presentation:
Elbow extended
Erb’s Palsy
Affected muscles: and wrist flexion
(C5-C6)
Shoulders and but normal grasp
Upper arm
Lower Presentation:
Weak grasp and
Affected muscles: affected limb
Forearm and hand small. Horner’s
Klumpke’s Palsy
syndrome may
(C7-T1)
present due to
interruption of fiber
to cervical
sympathetic trunk
Secondary to Post mastectomy
 Known history of radiation treatment
 Tingling sensation to fingers and arms
Secondary to Metastasis