Peripheral Neuropathies & Other Disorders
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dr. Yetty Hutahaean, Sp.S
Kuliah Modul-3 Blok 15
Fakultas Kedokteran Universitas Mulawarman
Rabu
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24 Nov
ember 20
22
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Disease or injury of peripheral sensory,
motor or autonomic nerves
May be pure motor, pure sensory or
mixed sensorimotor
May occur as mononeuropathy,
polyneuropathy or multifocal neuropathy
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Mononeuropathy
Clinical syndrome of idiopathic acute
unilateral facial paralysis
Incidence 1: 5000 people
More common during pregnancy &
elderly
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Unilateral facial weakness/facial drop,
most around mouth
↓ forehead wrinkling & raising
eyebrow, incomplete eyelid closure
Patients may report exposure to cold
preceded their symptpms
Facial numbness or stiffness without
objective sensory deficit
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Mild-moderate pain at the angel of jaw
May be loss of teste 2/3 ant tongue
Decrease tearing and ipsilateral
hyperacusis
Not life-threatening
may have severe
functional, aesthetic & psycological
consequences
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Pharmacotherapy
- Prednisone 1mg/kg/day for a week
- Antiviral (still controversial):
acyclovir 400mg,5x/day, 7-10 days
if renal function is normal
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Surgical Therapy: decompression as acute
therapy based on hypotesis ‘neuronal
swelling within temporal bone’
highly
invasive & risk permanent hearing loss
Suportive Care
- Artificial tears & ophthalmic ointment
- Glasses or google
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60 - 80% cases
complete recovery in 1-2
months without treatment
90% achieve complete recovery with
corticosteroid
5% cases
permanent sequele
During recovery period, may experience
involuntary activation of facial muscle in
ipsilateral region as a result of aberrant
reinnervation (synkinesias & crocodile
tear)
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Mononeuropathy
Carpal tunnel, formed by carpal bones
& coverd ventrally by flexor
retinaculum
Prone to compression with repetitive
flexion & extension
Most common occupational diseases
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Pain, paresthesias or numbness in the
first 3 digits
Worsen w/ repetitive/sustained wrist
flexion or extension
Intermittent
constant
Severe condition: hand weakness
thenar flattening
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Tinel & Phalen test (+)
Medical condition that may increase
risk: diabetes mellitus, hypothyroidism,
pregnancy, rheumatoid arthritis, obesity
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Electromyography & nerve conduction
studies
Motor & sensory conduction time
through the carpal tunnel
loss motor
amplitudes : worrisome sign
Blood studies to asses for the risk factor
mention above
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Pharmacotherapy
- anti-inflammatory agents
- Vitamin B6
- Short course of oral prednisone
- local corticosteroid injection
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Conservative therapy: wrist splinting in
netral position at night & during
activities
Surgical: carpal tunnel release surgery
transection of the transverse carpal
ligament
excellent success w/ few
complication
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Acquired polyneuropathy
Group of immune-mediated disorders
Annual incidence 1-2 cases per 100.000
people
Most common form: acute
inflammatory demyelinating
polyradiculoneuropathy (AIDP)
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Progressive weakness of extremities
w/ attenuation or loss of reflexes
Target antigen susp on myelin sheat
Patologically, demyelination begin in
the proximal nerves
distal
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Upper respiratory infection,
gastrointestinal infection or non
specific febrile illness, precedes
neurologic symptoms
Campylobacter jejuni: most frequently
identified organism
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Subtypes:
1. Acute inflammatory demyelinating
polyradikuloneuropathy (AIDP)
2. Acute motor axonal neuropathy
(AMAN)
3. Acute motor sensory axonal
neuropathy (AMSAN)
4. Miller fisher syndorme
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Often begins 1-3 weeks after infection
70% patients initially have parestesias or
numbness in hands & feet
symmetris
weakness (typically ascending)
progress days – weeks
Paralysis max about 2 weeks (50%) & 1
month in > 90% pts.
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Respiratory paralysis may rapidly appear
(±
¼ AIDP)
necessitating intubation &
mechanical ventilation
Autonomic nervous system involvement:
dangerous fluctuation od blood pressure
or cardiac arrythmia
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Examination:
- symmetric flaccid weakness
- normal sensation, despite sensory
symptom
- impending respiratory failure
- autonomic involvement: cardiac
arrythmia, BP fluctuation,
flushing,
sweating, abnormal GI
motility
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Lumbal puncture:
- CSF protein ↑ few days after
onset, peak in 4-6 weaks
- cell count normal/ mild
lymphocytic pleocytosis
cyto-albumin dissociation
Nerve conduction studies
EMG : ↓ motor unit recruitment
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Intravenous immunoglobulin: IVIG 0,4
g/kg/day for 5 days
Plasmapheresis: 5-6 exchanges over 1-2
weeks
Combination of both gives no additional
benefit
Randomized trials of oral & intravenous
corticosteroid: failed to show benefit
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Most patients return to normal function
After progression stops, symptoms
usually plateu for 2-4 weeks
gradual
recovery
20-25% require mechanical ventilation
5% die
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Residual motor weakness in 25% after 1
year
Poor prognostic factors: Older age,
ventilatory support, rapid progression
(<7 days), low motor amplitude
< 20%
probability of walkin independently at 6
months
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Most common of neuromuscular junction
disordes
Acquired, predominantly antibody
mediated autoimmune disease
Antibodies targeted against nicotinic
acetylcholine receptor (AChR)
Prevalence 1: 10.000-20.000 people
Comorbid thyroid disease (> 10%)
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Fluctuating, fatigable weakness of
commonly used muscles
Hallmark features: ptosis, diplopia,
disarthria, dysphagia, respiratory &
limb muscles weakness
Half of patients present w/ ocular
findings, usually bilateral, asymmetric
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Myasthenia crisis: respiratory
symptoms in conjunction with severe
bulbar symptom (15-20% patients)
mechanical ventilation
Risk ↑ pregnant women during first
trimester, improve during second &
third trimester
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Tensilon (edrophonium) test: 1mg iv
3mg iv (3x)
Observe respon in 30-60’’
(negative if no response until 2’)
Laboratory studies:
- AChR binding antibody
- AChR modulating antibody
Electrodiagnostic studies
Asses the present of tymoma by chest
CT-Scan/MRI
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Symptomatic treatment
- Acetycholinesterase inhibitor
(pyridostigmin, at least 3-4x daily)
Immunosupressive treatment
- Thymectomy
- Medical therapy: corticosteroid
- Plasmapheresis
- IVIG
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80%
general myasthenic
Cholinesterase inhibitor, low-
dosecorticosteroid may control
symptom
Patients w/ thymoma
more
aggressive disease course
Peripheral Neuropathy is a condition affecting peripheral nerves, leading to sensory, motor, or autonomic nerve damage. It can manifest in various forms, including mononeuropathy, polyneuropathy, or multifocal neuropathy. Bell's Palsy, a type of mononeuropathy, is characterized by acute unilateral facial paralysis and is more common in certain populations. Clinical findings may include facial weakness, numbness, pain, and other symptoms. Treatment typically involves pharmacotherapy such as Prednisone and antiviral medication.
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Presentation Transcript
Peripheral Peripheral Neuropathies & Other Neuropathies & Other Disorders Disorders dr. Yetty Hutahaean, Sp.S Kuliah Modul-3 Blok 15 Fakultas Kedokteran Universitas Mulawarman Rabu, 24 November 2022
Peripheral Neuropathy Peripheral Neuropathy Disease or injury of peripheral sensory, motor or autonomic nerves May be pure motor, pure sensory or mixed sensorimotor May occur as mononeuropathy, polyneuropathy or multifocal neuropathy
Bell Palsy Bell Palsy
General Consideration General Consideration Mononeuropathy Clinical syndrome of idiopathic acute unilateral facial paralysis Incidence 1: 5000 people More common during pregnancy & elderly
Clinical Findings Clinical Findings Unilateral facial weakness/facial drop, most around mouth forehead wrinkling & raising eyebrow, incomplete eyelid closure Patients may report exposure to cold preceded their symptpms Facial numbness or stiffness without objective sensory deficit
Clinical Findings Clinical Findings Mild-moderate pain at the angel of jaw May be loss of teste 2/3 ant tongue Decrease tearing and ipsilateral hyperacusis Not life-threatening functional, aesthetic & psycological consequences may have severe
Treatment Treatment Pharmacotherapy - Prednisone 1mg/kg/day for a week - Antiviral (still controversial): acyclovir 400mg,5x/day, 7-10 days if renal function is normal
Treatment Treatment Surgical Therapy: decompression as acute therapy based on hypotesis neuronal swelling within temporal bone invasive & risk permanent hearing loss highly Suportive Care - Artificial tears & ophthalmic ointment - Glasses or google
Prognosis Prognosis 60 - 80% cases months without treatment complete recovery in 1-2 90% achieve complete recovery with corticosteroid 5% cases permanent sequele During recovery period, may experience involuntary activation of facial muscle in ipsilateral region as a result of aberrant reinnervation (synkinesias & crocodile tear)
Carpal CarpalTunnel Tunnel
General Consideration General Consideration Mononeuropathy Carpal tunnel, formed by carpal bones & coverd ventrally by flexor retinaculum Prone to compression with repetitive flexion & extension Most common occupational diseases
Clinical Findings Clinical Findings Pain, paresthesias or numbness in the first 3 digits Worsen w/ repetitive/sustained wrist flexion or extension Intermittent constant Severe condition: hand weakness thenar flattening
Clinical Findings Clinical Findings Tinel & Phalen test (+) Medical condition that may increase risk: diabetes mellitus, hypothyroidism, pregnancy, rheumatoid arthritis, obesity
Diagnostic Studies Diagnostic Studies Electromyography & nerve conduction studies Motor & sensory conduction time through the carpal tunnel amplitudes : worrisome sign loss motor Blood studies to asses for the risk factor mention above
Treatment Treatment Pharmacotherapy - anti-inflammatory agents - Vitamin B6 - Short course of oral prednisone - local corticosteroid injection
Treatment Treatment Conservative therapy: wrist splinting in netral position at night & during activities Surgical: carpal tunnel release surgery transection of the transverse carpal ligament excellent success w/ few complication
Tarsal TarsalTunnel Tunnel
Guillain Guillain- -Barre Barre
General Consideration General Consideration Acquired polyneuropathy Group of immune-mediated disorders Annual incidence 1-2 cases per 100.000 people Most common form: acute inflammatory demyelinating polyradiculoneuropathy (AIDP)
General Consideration General Consideration Progressive weakness of extremities w/ attenuation or loss of reflexes Target antigen susp on myelin sheat Patologically, demyelination begin in the proximal nerves distal
General Consideration General Consideration Upper respiratory infection, gastrointestinal infection or non specific febrile illness, precedes neurologic symptoms Campylobacter jejuni: most frequently identified organism
General Consideration General Consideration Subtypes: 1. Acute inflammatory demyelinating polyradikuloneuropathy (AIDP) 2. Acute motor axonal neuropathy (AMAN) 3. Acute motor sensory axonal neuropathy (AMSAN) 4. Miller fisher syndorme
Clinical Findings Clinical Findings Often begins 1-3 weeks after infection 70% patients initially have parestesias or numbness in hands & feet weakness (typically ascending) progress days weeks symmetris Paralysis max about 2 weeks (50%) & 1 month in > 90% pts.
Clinical Findings Clinical Findings Respiratory paralysis may rapidly appear ( AIDP) necessitating intubation & mechanical ventilation Autonomic nervous system involvement: dangerous fluctuation od blood pressure or cardiac arrythmia
Clinical Findings Clinical Findings Examination: - symmetric flaccid weakness - normal sensation, despite sensory symptom - impending respiratory failure - autonomic involvement: cardiac arrythmia, BP fluctuation, flushing, sweating, abnormal GI motility
Diagnostic Studies Diagnostic Studies Lumbal puncture: - CSF protein few days after onset, peak in 4-6 weaks - cell count normal/ mild lymphocytic pleocytosis cyto-albumin dissociation Nerve conduction studies EMG : motor unit recruitment
Treatment Treatment Intravenous immunoglobulin: IVIG 0,4 g/kg/day for 5 days Plasmapheresis: 5-6 exchanges over 1-2 weeks Combination of both gives no additional benefit Randomized trials of oral & intravenous corticosteroid: failed to show benefit
Prognosis Prognosis Most patients return to normal function After progression stops, symptoms usually plateu for 2-4 weeks recovery gradual 20-25% require mechanical ventilation 5% die
Prognosis Prognosis Residual motor weakness in 25% after 1 year Poor prognostic factors: Older age, ventilatory support, rapid progression (<7 days), low motor amplitude probability of walkin independently at 6 months < 20%
Myasthenia Myasthenia
General Consideration General Consideration Most common of neuromuscular junction disordes Acquired, predominantly antibody mediated autoimmune disease Antibodies targeted against nicotinic acetylcholine receptor (AChR) Prevalence 1: 10.000-20.000 people Comorbid thyroid disease (> 10%)
Clinical Findings Clinical Findings Fluctuating, fatigable weakness of commonly used muscles Hallmark features: ptosis, diplopia, disarthria, dysphagia, respiratory & limb muscles weakness Half of patients present w/ ocular findings, usually bilateral, asymmetric
Clinical Findings Clinical Findings Myasthenia crisis: respiratory symptoms in conjunction with severe bulbar symptom (15-20% patients) mechanical ventilation Risk pregnant women during first trimester, improve during second & third trimester
Diagnostic Studies Diagnostic Studies Tensilon (edrophonium) test: 1mg iv 3mg iv (3x) Observe respon in 30-60 (negative if no response until 2 ) Laboratory studies: - AChR binding antibody - AChR modulating antibody Electrodiagnostic studies Asses the present of tymoma by chest CT-Scan/MRI
Treatment Treatment Symptomatic treatment - Acetycholinesterase inhibitor (pyridostigmin, at least 3-4x daily) Immunosupressive treatment - Thymectomy - Medical therapy: corticosteroid - Plasmapheresis - IVIG
Prognosis Prognosis 80% general myasthenic Cholinesterase inhibitor, low- dosecorticosteroid may control symptom Patients w/ thymoma aggressive disease course more
Radiculopathy Radiculopathy
Cauda CaudaEquina Equina
Brachial Brachial
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