Aula de monitorização de Nervos em Cirurgia de Cabeça e Pescoço.

1. Neuromonitorização em
Cirurgia de Cabeça e Pescoço
DR. LEONARDO RANGEL

2. “ Always start with the why”

3. “ Always start with the why”

4. Porque !!!
Principal morbidade da
cirurgias de cabeça e
pescoço são as sequelas
causadas pelas lesões
nervosas

5. AGENDA
Fisiologia
Anatomia
Tipos de Lesão
Tipos de Monitorização

6. Nobody likes the Basics

7. Everyone want’s to play

8. TecnicaCirúrgica
Anatomia
Fisiologia
TiposdeLesão

9. Fisiologia

10. • Physiology of the Nervous Impulse

11. • Anatomy : Peripheric Nerves

12. • Eletro - neuro - mio - graphy
• Electric Stimulus
• Capture Eletrodes

13. • Amplitude
• Latency
• Duration

14. Compressive
Lesions
was first introduced by Kimura (1979). Other authors
found that inching was the most sensitive technique to
detect CTS (White et al., 1988).
across the carpal tunnel (Buchthal a
1971). Orthodromic or antidromic sensor
duction velocity from palm to wrist or w
Fig. 19.6. Motor nerve conduction of both median nerves and right ulnar nerve. Prolonged distal motor latencies
nerves at the wrist, more pronounced at the right side. Reduced compound muscle action potential amplitude
N. Median
Left
Right

15. Surgical Technique
Anatomy

16. Left RLN
L1C R1
Right RLN
The International RLN Anatomic
Classification System
Gregory W. Randolph, Che-Wei Wu,
Gianlorenzo Dionigi, Dipti Kamani, Rahul R. Modi,
Feng-Yu Chiang, and Jean François Henry
12
“People see what they are prepared to see”—Ralph Waldo Emerson journals 1863
The Recurrent
and Superior
Laryngeal Nerves
GregoryW.Randolph
Editor
123

17. • Vagus N.
• Laryngeal
Recurrent N.
• Exteranl Branch of
Superior Laryngeal N.
Left RLN
L1C R1
Right RLN

18. • N. Vagus
12 The International RLN Anatomic Classification System

19. 128
Table 12.1 The RLN anatomical classification and the estimated prevalence of each class
Class Descriptiona
Estimated prevalence
I. Left recurrent laryngeal nerve class
L1 Normal trajectory 95 %
L2a Abnormal acquired-lateral 5 %
L2b Abnormal acquired-ventral <1 %
L3 Abnormal embryologic - left nonrecurrent
(NRLN)
0.04 %
II. Right recurrent laryngeal nerve class
R1 Normal trajectory 90 %
R2a Abnormal acquired-medial 5–10 %
R2b Abnormal acquired-ventral <1 %
R3 Abnormal embryologic-right nonrecurrent
(NRLN)
0.5–1 %
III. Clinically important neural feature
Anatomical
F-Fixed/splayed/entrapped Capsular Association through fascial bands,
vessels, or goiterous change
With substernal goiter 15 % [7]
I-Invaded Neural invasion With cancer <5 % [7]
L-posterior Ligament of Berry
entrapment
Posterior ligament of Berry or associated
vessel neural entrapment
10 % [7]
B-branched Extralaryngeal RLN branching 24.3–72 % [15–19]
T-Thin caliber nerve Neural caliber <1 mm <2.5 % [20, 21]
Dynamic
Loss of electrophysiologic monitoring
G.W. Randolph et al.
L1
B
SLN internal
branch
SLN external
branch
RLN in
tracheoesophagealgroove
L
la
n
L1
L1
C
R1

20. 128
Table 12.1 The RLN anatomical classification and the estimated prevalence of each class
Class Descriptiona
Estimated prevalence
I. Left recurrent laryngeal nerve class
L1 Normal trajectory 95 %
L2a Abnormal acquired-lateral 5 %
L2b Abnormal acquired-ventral <1 %
L3 Abnormal embryologic - left nonrecurrent
(NRLN)
0.04 %
II. Right recurrent laryngeal nerve class
R1 Normal trajectory 90 %
R2a Abnormal acquired-medial 5–10 %
R2b Abnormal acquired-ventral <1 %
R3 Abnormal embryologic-right nonrecurrent
(NRLN)
0.5–1 %
III. Clinically important neural feature
Anatomical
F-Fixed/splayed/entrapped Capsular Association through fascial bands,
vessels, or goiterous change
With substernal goiter 15 % [7]
I-Invaded Neural invasion With cancer <5 % [7]
L-posterior Ligament of Berry
entrapment
Posterior ligament of Berry or associated
vessel neural entrapment
10 % [7]
B-branched Extralaryngeal RLN branching 24.3–72 % [15–19]
T-Thin caliber nerve Neural caliber <1 mm <2.5 % [20, 21]
Dynamic
G.W. Randolph et al.
R1R1
SLN internal
branch
SLN external
branch
RLN
Right
vagus
nerve
Right
laryngeal
nerve
LB
A

21. Facial

22. Facial
Extracraniano
Iatrogênico
Trauma
Grande Morbidade :
Estética
Funcional ( ocular, disfagia, fonação)

23. Facial
Extracraniano

25. Hipoglosso

26. Hipoglosso
Sínd de TAPIA (1905)
Antonio Garcia Tapia - El matador syndrome
Lesão de Hipoglosso
Lesão do N Recorrente

27. Hipoglosso

28. Acessório
Maior Causa = Iatrogênica
Bx Linfonodo
Esvaziamento
Tumores deste triangulo
Cir. Carótidas
Cir. De Jugular
Facelift
Trauma

29. Acessório

30. Acessório
Esvaziamento Cervical
Radical 46%
Seletivo 42%
Modificado 25%

31. Marginal

32. Marginal
Maior Causa = Iatrogênica
Bx Linfonodo
Esvaziamento
Mecanismo :
Dissecção
Compressão

33. Tipos de Lesão

34. Seddon Types of Lesion Sunderland
Neurapraxis Segmentar Desmielination
1o grade
Axonotmesis Wound Axon with preserved Endoneuron 2o grade
Axonotmesis
Severed Axon with Endoneuron lesion.
Perineuron and Fascicle Preserved
3o grade
Axonotmesis Just Epineuron preserved 4o grade
Neurotmesis Total loss of continuity 5o grade

35. Seddon Sunderland
Neurapraxis
1o Grade
Axonotmesis 2o Grade
Axonotmesis 3o Grade
Axonotmesis 4o Grade
Neurotmesis 5o Grade
Fig. 1. Diagrammatic representation of the five degrees of nerve injury. (1) Segmental demyelination causing conduction block but no damag
and no Wallerian degeneration, (2) damage to the axon severe enough to cause Wallerian degeneration and denervation of the target organ
intact endoneurium and good prospects for axon regeneration, (3) disruption of the axon and its endoneurial sheath inside an intact perineu
W.W. Campbell / Clinical Neurophysiology 119 (2008) 1951–1965
Epineuron
Perineuron
Endoneuron
Axon

36. • Neurapraxis
• Mild form of lesion
• Conduction distal to lesion
• Recovery after re-mielinization
• No Muscle atrophy
• Recovery after hours until 6 Mo
• In general 6-12 weeks
ence of pseudomeningoceles is further evidence favoring
root avulsion. These entities often do not occur in pure
degree lesion, neurogenic atrophy does develop, sometimes
rapidly, and the Tinel sign moves distally at approximately
Fig. 1. Diagrammatic representation of the five degrees of nerve injury. (1) Segmental demyelination causing conduction block but no damage to the axon
and no Wallerian degeneration, (2) damage to the axon severe enough to cause Wallerian degeneration and denervation of the target organ, but with an
intact endoneurium and good prospects for axon regeneration, (3) disruption of the axon and its endoneurial sheath inside an intact perineurium, loss of
integrity of the endoneurial tubes will limit axon regeneration, (4) disruption of the fasciculi, with nerve trunk continuity maintained only by epineurial
tissue, severe limitation of axon regeneration, formation of a mass of misdirected axons (neuroma in continuity), (5) transaction of the entire nerve trunk.
(Modified from Sunderland S. Nerves and nerve injuries, 2nd ed. Baltimore: ***Williams and Wilkins, 1978.)
W.W. Campbell / Clinical Neurophysiology 119 (2008) 1951–1965 1957

37. • Axonotmesis
• Caused by: laceration, contusion, stretch
, thermal or electric lesion.
• Causes Wallerian Degeneration !
• Nerve Structure as scaffold
• Time of recovery depends on the
distance of the lesion to the target organ
ence of pseudomeningoceles is further evidence favoring
root avulsion. These entities often do not occur in pure
form, as the forces required to avulse a root also often
severely injure the plexus, abolishing the sensory potential.
So the absence of a sensory potential does not alone prove
the absence of a root avulsion.
Physical examination, including eliciting Tinel sign, is
useful in following patients with peripheral nerve injury.
A flicker of movement or some degree of preserved sensa-
tion indicates that the lesion is incomplete. Substitute or
‘‘trick” movements often make the determination challeng-
ing. A trick movement is when the patient uses a normal
muscle or movement to substitute for a weak muscle. For
instance, the ‘‘bartender’s sign” is when a patient with
degree lesion, neurogenic atrophy does develop, sometimes
rapidly, and the Tinel sign moves distally at approximately
1 in./month, indicating advancement of the axonal growth
cone. With a third degree lesion, there is atrophy, and the
Tinel sign does progress distally, but at a slower than
expected rate. With fourth degree and fifth degree lesions,
atrophy is usually severe and rapid, but the Tinel sign never
migrates distally. Mixed lesions are relatively common,
with some degree of neurapraxia accompanied by variable
degrees of axonal damage. Some sources refer to mixed
lesions as a Sunderland sixth degree lesion, although Sun-
derland did not include such a category. With clinically
and electrophysiologically complete lesions, the return of
function as gauged by a flicker of movement on physical
Fig. 1. Diagrammatic representation of the five degrees of nerve injury. (1) Segmental demyelination causing conduction block but no damage to the axon
and no Wallerian degeneration, (2) damage to the axon severe enough to cause Wallerian degeneration and denervation of the target organ, but with an
intact endoneurium and good prospects for axon regeneration, (3) disruption of the axon and its endoneurial sheath inside an intact perineurium, loss of
integrity of the endoneurial tubes will limit axon regeneration, (4) disruption of the fasciculi, with nerve trunk continuity maintained only by epineurial
tissue, severe limitation of axon regeneration, formation of a mass of misdirected axons (neuroma in continuity), (5) transaction of the entire nerve trunk.
(Modified from Sunderland S. Nerves and nerve injuries, 2nd ed. Baltimore: ***Williams and Wilkins, 1978.)

38. Wallerian
Degeneration

39. • Axonotmesis
• Caused by: laceration, contusion, stretch
, thermal or electric lesion.
• Causes Wallerian Degeneration !
• Nerve Structure as scaffold
• Time of recovery depends on the
distance of the lesion to the target organ
ence of pseudomeningoceles is further evidence favoring
root avulsion. These entities often do not occur in pure
form, as the forces required to avulse a root also often
severely injure the plexus, abolishing the sensory potential.
So the absence of a sensory potential does not alone prove
the absence of a root avulsion.
Physical examination, including eliciting Tinel sign, is
useful in following patients with peripheral nerve injury.
A flicker of movement or some degree of preserved sensa-
tion indicates that the lesion is incomplete. Substitute or
‘‘trick” movements often make the determination challeng-
ing. A trick movement is when the patient uses a normal
muscle or movement to substitute for a weak muscle. For
instance, the ‘‘bartender’s sign” is when a patient with
degree lesion, neurogenic atrophy does develop, sometimes
rapidly, and the Tinel sign moves distally at approximately
1 in./month, indicating advancement of the axonal growth
cone. With a third degree lesion, there is atrophy, and the
Tinel sign does progress distally, but at a slower than
expected rate. With fourth degree and fifth degree lesions,
atrophy is usually severe and rapid, but the Tinel sign never
migrates distally. Mixed lesions are relatively common,
with some degree of neurapraxia accompanied by variable
degrees of axonal damage. Some sources refer to mixed
lesions as a Sunderland sixth degree lesion, although Sun-
derland did not include such a category. With clinically
and electrophysiologically complete lesions, the return of
function as gauged by a flicker of movement on physical
Fig. 1. Diagrammatic representation of the five degrees of nerve injury. (1) Segmental demyelination causing conduction block but no damage to the axon
and no Wallerian degeneration, (2) damage to the axon severe enough to cause Wallerian degeneration and denervation of the target organ, but with an
intact endoneurium and good prospects for axon regeneration, (3) disruption of the axon and its endoneurial sheath inside an intact perineurium, loss of
integrity of the endoneurial tubes will limit axon regeneration, (4) disruption of the fasciculi, with nerve trunk continuity maintained only by epineurial
tissue, severe limitation of axon regeneration, formation of a mass of misdirected axons (neuroma in continuity), (5) transaction of the entire nerve trunk.
(Modified from Sunderland S. Nerves and nerve injuries, 2nd ed. Baltimore: ***Williams and Wilkins, 1978.)

40. • Neurotmesis
• Most Severe Form
• Dismal recovery chances without intervention
ence of pseudomeningoceles is further evidence favoring
root avulsion. These entities often do not occur in pure
form, as the forces required to avulse a root also often
severely injure the plexus, abolishing the sensory potential.
So the absence of a sensory potential does not alone prove
the absence of a root avulsion.
Physical examination, including eliciting Tinel sign, is
useful in following patients with peripheral nerve injury.
A flicker of movement or some degree of preserved sensa-
tion indicates that the lesion is incomplete. Substitute or
‘‘trick” movements often make the determination challeng-
ing. A trick movement is when the patient uses a normal
muscle or movement to substitute for a weak muscle. For
instance, the ‘‘bartender’s sign” is when a patient with
weak elbow flexion pulls the elbow backwards when the
examiner tries to examine the biceps (Campbell, 2005).
With a first degree lesion, the Tinel sign remains focal over
the area of abnormality, and, although there may be weak-
ness, muscle atrophy, except for that due to disuse, does
not develop because there is no axon loss. With a second
degree lesion, neurogenic atrophy does develop, sometimes
rapidly, and the Tinel sign moves distally at approximately
1 in./month, indicating advancement of the axonal growth
cone. With a third degree lesion, there is atrophy, and the
Tinel sign does progress distally, but at a slower than
expected rate. With fourth degree and fifth degree lesions,
atrophy is usually severe and rapid, but the Tinel sign never
migrates distally. Mixed lesions are relatively common,
with some degree of neurapraxia accompanied by variable
degrees of axonal damage. Some sources refer to mixed
lesions as a Sunderland sixth degree lesion, although Sun-
derland did not include such a category. With clinically
and electrophysiologically complete lesions, the return of
function as gauged by a flicker of movement on physical
examination or the return of motor unit action potentials
(MUAPs) by EMG examination indicates that reinnerva-
tion is occurring. The EMG is more sensitive than the
physical examination for detecting early reinnervation, so
return of MUAPs on needle examination in the muscle
closest to the injury site is typically the first evidence of
Fig. 1. Diagrammatic representation of the five degrees of nerve injury. (1) Segmental demyelination causing conduction block but no damage to the axon
and no Wallerian degeneration, (2) damage to the axon severe enough to cause Wallerian degeneration and denervation of the target organ, but with an
intact endoneurium and good prospects for axon regeneration, (3) disruption of the axon and its endoneurial sheath inside an intact perineurium, loss of
integrity of the endoneurial tubes will limit axon regeneration, (4) disruption of the fasciculi, with nerve trunk continuity maintained only by epineurial
tissue, severe limitation of axon regeneration, formation of a mass of misdirected axons (neuroma in continuity), (5) transaction of the entire nerve trunk.
(Modified from Sunderland S. Nerves and nerve injuries, 2nd ed. Baltimore: ***Williams and Wilkins, 1978.)

41. Recovery Mechanism

42. • Recovery Mechanisms
• Re-mielinization - mainly neurapraxia
• Lateral Sprouts - 20-30% of Nerve Lesion
• Regeneration of site of lesion- 90% n lesion

43. • Recovery Mechanisms
• Re-mielinization - mainly neurapraxia
• Lateral Sprouts - 20-30% of Nerve Lesion
• Regeneration of site of lesion- 90% n lesion

44. • Recovery Mechanisms
• Re-mielinization - mainly neurapraxia
• Lateral Sprouts - 20-30% of Nerve Lesion
• Regeneration of site of lesion- 90% n lesion

45. • Conclusion :
• Nerve Anatomy and physiology is vital to
prevent lesions
• Attention to Thyroid anatomy and variations
• laceration, contusion, stretch , thermal and
electric lesions are the mechanism of lesion