peripheral neuropathy aida

8/7/2019 Peripheral Neuropathy Aida

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PERIPHERAL NEUROPATHYCLINICAL APPROACH


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UMNWeakness entire limb/side

Hypertonia /SpasticityBrisk reflex

Barbinski +ve

No/slight muscle atrophy

Clonus

LMNParalysis muscle in discrete

areaHypotonia / Flacidity

Reflex absent /normal

Muscle wasting (atrophy)

fasciculation

Spinal cord

contain both UMNand LMN, if

damage :

UMN /LMN /

combination


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Anterior horn cell Peripheral nerve NMJ Muscle

Hypotonia Yes Yes Yes Yes

Wasting (atrophy) Yes Yes Yes Yes

Flaccidity

(paralysis)

Yes (a group of

muscle)

Yes Yes Yes

Fasciculation

(twitching of

muscle)

Yes Yes Yes Yes

Deep tendon

reflex

No No Yes Yes

Fatigue Yes No

Motor Yes Yes Yes Yes

Sensory No Yes No No


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Different type of nerve fibre ( Type A, Type

B,Type C) had different type of function.

Depending on which type of nerve fibre that is

damage, their function will be gone.


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Mechanism damage to peripheral nerve

1. Demyelination

2. Axonal degeneration3. Wallerian degeneration

4. Compression

5. Infarction6. Infiltration


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Peripheralneuropathysymptoms

Motor.

Weakness(usually start

distally)Cramps

Fasciculation

Tremor

Autonomic

Sensory

Positive phenomena

Paresthesia, Dysesthesia,Hyperalgesia, Causalgia-spontaneous burning pain,

Lightning pain

Negative phenomena

Hyposthesisa, Anesthesia

Ataxia


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Peri her lneur th

si n

Tr hicch n es-ulcer/j ints/ h ir

l ss/brittlen il/c ld blueextremities

P.N.Thickenin

Tenderness

Tinnels si n

Sens r .Im ired in cut neous

Nerve distribution

Dist l s mmetric Glovend Stockin distribution

Derm tom l distribution

Preferenti l loss ofcert in mod lities

Motor.W stin

F scicul tion

H otoni

Weakness

Absent DTR


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D- diabetes

A- alcohol

N- nutritional

G- Guillain-barre

T- trauma

H- hereditary E- environmental ( toxin / drugs )

R- rheumatic (collagen vascular)

A- amyloid P- paraneoplastic

I- infection

S- systemic dz

T- tumours

C

A

U

SE

S


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History

Onset

o Acute / Sub acute / Chronic

Course

o Relapsing or not

Function disturbance

o Sensory / Motor / Sensory motor / Autonomic

Systemic illness

o Endocrine / Metabolic

Drug history

Exposure to toxins

Family history


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Age of onset

Neonatal- development , birth injury

Childhood / early adult hood hereditary basis ,

inflammatory

Later life metabolic, toxic , inflammatory,

neoplasm, occupational


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Occupational history

Carpal tunnel syndrome- repetitive motion

Exposure to substance carbon disulfide ,

acrylamide, lead, etc


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Past medical hx

Metabolic diabetes mellitus , etc

Neoplasm spinal cord compression , etc

Connective tissue disorder polyarteritis nodosa,rheumatoid arthritis (mononeuropathy multiplex )

AIDS distal , symmetric , sensory polyneuropathy


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Drug and alcohol hx

Quinolones

Vincristine

Cisplatin Isoniazid

Metronidazole


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Family hx

Hereditary basis CMT , porphyria , etc


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Pattern of deficit

Cranial nerve involvement Diabetes mellitus,

GBS, HIV/AIDS , etc

Most neuropathy begin distally , except-

Chronic inflammatory demyelinating

polyradiculoneuropathy ,Diabetes mellitus , etc

Predominant upper limbs GBS , Diabetes mellitus


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Predominantly motor : GBS , lead poisoning, CMT

Predominantly sensory: DM, uraemia , leprosy

Autonomic involvement : Diabetic neuropathy,Amyloidosis , etc


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Physical examination


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Sensory nerve involvement

Sensory loss is symmetrical Stocking and glove distribution

Involvement of large fibers (include motor axons and thesensory axons for vibration sense, proprioception and

light touch) vibration and joint senses, romberg test +ve

involvement of small fibers (autonomic fibers andsensory axons responsible for light touch, pain and

temperature ) pin prick sensation and temperature


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Others

Neuropahtic pain

Trophic changes

Cold blue extremities

Cutaneous hair loss


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Motor nerve involvement

Features of lower motor neuron

Muscle wasting (in axonal but absent in demyelinating

neuropathies)

Fasciculation (irregular twitches of groups of musclefibres due to anterior horn cells disease)

Weakness (proportional to no of affected neurons)

Longest neuron being the most vulnerable


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Autonomic fibre involvement

orthostatic hypotension without a compensatory rise in

heart rate

Fainting spells

Bladder,bowel,sexual dysfunction

Systemic disease

lymphadenopathy, hepatomegaly or splenomegaly andskin lesions


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Reflexes

Decreased / lost (early to diminished when power

and muscle appear normal)

Distal generally will lost first


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Cranial nerve examination

CN 1 (anosmia) = Refsum's disease and vitamin B12deficiency

CN 2 (impaired pupillary light reflex) = may indicateparasympathetic involvement which may occur in diabetic

neuropathy and GB syndrome. CN 3,4,6 (external ophthalmoplegia)= Miller Fisher

syndrome

CN 5 (sensory loss) = Sjogren's syndrome

(lower cranial nerve palsy) = Kennedy'ssyndrome.

CN 7 (facial weakness) = GB syndrome and bells palsy


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Diagnostic assessment

MimickersHigh cervical lesion

If Gracilis column first, then the Cuneatecolumn, symptoms develop in L.Lfollowed by U.L

Preservation of Ankle Jerk. Clueagainst neuropathyPsychogenicMyasthenia

MimickersHigh cervical lesion

If Gracilis column first, then the Cuneatecolumn, symptoms develop in L.Lfollowed by U.L

Preservation of Ankle Jerk. Clueagainst neuropathyPsychogenicMyasthenia


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Investigations


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Step-I

FBC, ESR Urine-Glucose,

Proteins FBS, RFT, LFT, TFT X-ray Chest Electro diagnostic

Study

Step-II

Serum proteinElectrophoresis

ImmunologicalInvestigations

Step III

-Urine Bence Jones protein

-GTT

-CSF

-Immunology- HIV,antineuralantibody,antigangliosideantibody

-Search for ca

-Nerve biopsy

-Molecular genetic study

No such thing as routine study- tailor made for each patient

Even after a thorough work up, no cause identified in 15-20%


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Confirm the presence of Neuropathy

Differentiate from NMJ / Muscle

Localize the pathology

Neurons/Root/ Plexus/ Nerves.

Mononeuritis/ Multiplex/

Polyneuropathy

Sensory/ Motor.

Characterize the pathology

Axonal/ Demyelinating

Severity and Chronicity Prognosis

Sub clinical involvement

Nerve conduction study


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Nerve Biopsy

Not required for most of routine cases

Might show the pathological changes-

but may not clinch an etiology.

May miss

Patchy lesions

Predominantly proximal conditions

Selective motor involvement

Indicated in cases of unknown etiology.

Expertise must be available Routine H&E, Axon/Myelin staining,

Immune studies, Teased fiber, EM


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Treatment


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GaneralProtection from trauma

Relief of painWithdraw toxin/drugs

Physiotheraphy

Rehabilitation

SurgeryEntrapmentneuropathy

Correction ofdeformities

SpecificTreat etiology

Treat systemic diseaseImmunosuppression

Immunomodulation


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Rehabilitation

Range Of Motion Exercises Neuromuscular Re-Education Training selective contraction of individual

or a group of muscles in a coordinated

sequence Sensory Re-Education. Goal is to restore adequate function Sensory system has great capacity for

regeneration Orthoses. Gait Training Occupational Therapy.


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Orthoses


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Gait training

peripheral neuropathy aida

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