Peripheral Neuropathy
Peripheral Neuropathy
Peripheral Neuropathy
Department of Neurology,
General hospital
Ningxia Medical University
Haining Li
Peripheral Neuropathy
Outline
Guillain-Barre Syndrome
Idiopathic facial palsy
Trigeminal neuralgia
OUTLINE
Anatomy
Pathological Processes
Clinical classifation
Symptoms
Investigation
Anatomy
Peripheral nerves are made up of numerous axons
bound together by three types of connective
tissue—endoneurium, perineurium, epineurium.
Peripheral nerve trunks contain myelinated and
unmyelinated fibres.
Crinial nerves
Spinal nerves
Pathological Processes
Wallerian degeneration: disintegration of
axons and myelin distal to the site of injury.
Axonal degeneration: distal dying of axons
and loss of myelin.
Neuronal degeneration: death of neuron body
Segmental demyelination
Normal Wallerian Axonal Neuronal Segmental
degeneration degeneration degeneration demyelination
Symptoms
Sensory disturbance
Motor deficits
Tendon reflexes
Autonomic disturbances
Others
Investigation
Nerve conduction velocity(NCV)
Electromyography(EMG)
Nerve biopsy
Blood tests
CSF examination
Trigeminal Neuralgia
Etiology and Pathology
A facial pain syndrome of unknown cause.
Demyelination
Clinical Features
It develops in middle to late life.
It consists of severe paroxysms electric-
shock-like pain, usually in the V3 and V2
division of the trigeminal nerve, lasting for
several seconds or minutes each time.
Involvement of V1 division or bilateral
disease occurs in less than 5% of cases.
Clinical Features
Occurrence during sleep is rare.
Painfree intervals may last for minutes to
weeks, but long-term spontaneous remission is
rare.
Sensory stimulation of trigger zones about the
cheek, nose, or mouth by touch, cold, wind,
talking, or chewing can precipitate the pain.
Clinical Features
Etiology: unknown
Pathology: edema, demyelination, axonal
degeneration
Clinical features
Onset
□ Occurs in any age, usually unilateral.
□ Paralysis: Progresses over 3 to 72 hours
□ Pain (50%): Near mastoid process
□ Excess tearing (33%)
□ Other: Hyperacusis; Dysgeusia
Clinical features
Signs
□ Facial weakness
Upper & Lower
Unilateral
Degree: Partial (30%); Complete (70%)
□ Stapedius dysfunction (33%): Hyperacusis
□ Lacrimation: mildly affected in some patients
□ Taste: No clinically significant changes in most
patients.
□ There should be no sensory loss in the face.
□ No abnormalities beyond the territory of the facial
nerve.
□ Hunt syndrome: caused by reactivation of herpes zoster
in the geniculate ganglion, consists of a severe facial palsy
associated with a vesicular eruption in the external
auditory canal and sometimes in the pharynx and other
parts of the cranial integument; often the eighth cranial
nerve is affected as well.
Clinical features
Prognosis better
□ Incomplete paralysis
□ Early improvement
□ Slow progression
□ Younger age
Clinical features
Prognosis better
□ Normal taste
□ Electrodiagnostic tests normal
Diagnosis and differential diagnosis
Diagnosis: acute onset with peripheral facial
palsy.
Differential diagnosis:
GBS
Treatment
Corticosteroids: prednisone 60mg qd po
dexamethason
VitaminB1,B12
Baclofen
Rehabilitation
Physiotherapy
Guillain-barré Syndrome
GBS is a kind of autoimmune disease
characterized by demyelination of peripheral
nerves and nerve roots. Inflammation of
lymphocytes and macrophages around small
vessels is the pathological feature.
Clinical classification
AIDP
AMAN
AMSAN
Fisher syndrome ( gait ataxia, areflexia,
and external ophthalmoplegia)
Unclassifiable GBS
Epidemiology