Shoulder:Nerve Problems Related to the Shoulder - Revision history

Alexandre.laedermann at 12:09, 3 June 2021

2021-06-03T12:09:55Z

Alexandre.laedermann at 11:59, 3 June 2021

2021-06-03T11:59:44Z

Alexandre.laedermann at 14:47, 16 February 2020

2020-02-16T14:47:27Z

Alexandre.laedermann: /* Brachial Plexitis (Parsonage-Turner Syndrome) */

2020-02-16T08:22:36Z

Brachial Plexitis (Parsonage-Turner Syndrome)

Alexandre.laedermann: /* Nerve constriction */

2020-02-16T08:21:36Z

Nerve constriction

Alexandre.laedermann: /* Nerve constriction */

2020-02-16T08:20:50Z

Nerve constriction

Alexandre.laedermann at 08:09, 16 February 2020

2020-02-16T08:09:02Z

Alexandre.laedermann at 07:49, 16 February 2020

2020-02-16T07:49:03Z

Alexandre.laedermann at 07:48, 16 February 2020

2020-02-16T07:48:26Z

Alexandre.laedermann at 07:45, 16 February 2020

2020-02-16T07:45:01Z

@@ Line 189: / Line 189: @@
 <br />
-There are several mechanisms of recovery following motor nerve damage: the resolution of conduction block during neurapraxis, muscle fiber hypertrophy during neuropraxis and axonotesis, intra-muscular collateral reinnervation during partial axonotesis and axonal regeneration from the site of lesion during partial and complete axonotesis and neurotesis.<ref>Robinson LR. Traumatic injury to peripheral nerves. Muscle Nerve 2000;23:863-73</ref>
+There are several mechanisms of recovery following motor nerve damage: the resolution of conduction block during neurapraxis, muscle fiber hypertrophy during neuropraxis and axonotesis, intra-muscular collateral reinnervation during partial axonotesis and axonal regeneration from the site of lesion during partial and complete axonotesis and neurotesis (Figure 1).<ref>Robinson LR. Traumatic injury to peripheral nerves. Muscle Nerve 2000;23:863-73</ref>
-[[File:Diapositive1.jpg|thumb|Recovery of strenght over time after nerve damage]]
+[[File:Diapositive1.jpg|thumb|Figure 1. Recovery of strength over time after nerve damage]]
-The following explanation may allow to understand the poor functional recovery occasionally observed: in axonotesis, axonal continuity is lost but the structures supporting the nerve are preserved. Axonal degeneration occurs on the distal portion of the axon from the site of the lesion. However, the preservation of the endoneural sheath allows the axons to direct their regeneration pedicles towards the originally innervated organ. This type of lesion should have a relatively good prognosis. However, the distance between the site of the lesion and the innervated organ vary. As the axon only regrows distally at an average speed of 1 mm per day, the motor plate and muscle fibers begin to atrophy before an axon reaches them. Finally, Schwann cells in the basement membrane degenerate after prolonged periods and the chances of an axon finding its way diminish for lesions located far from the target organ.<ref>Goldberg G, Goldstein H. AAEM case report 32: nerve injury associated with hip arthroplasty. Muscle Nerve 1998;21:519-27</ref> Time limits thus the potential for reinnervation. If the axon does not reach the motor plaque within two years, the degree of atrophy and scarring of the target muscle becomes so important that restoration of motor function is unlikely.<ref name=":2" />. Moreover, if the motor plate is affected, a sufficient number of axons is required for the muscles to be functional. So there is not always parallelism between electrical and clinical recovery. Indeed, it seems that for an electric reinnervation to be effective, it must be early; otherwise, recovery is still insufficient to restore a function.
+The following explanation may allow to understand the poor functional recovery occasionally observed: in axonotesis, axonal continuity is lost but the structures supporting the nerve are preserved. Axonal degeneration occurs on the distal portion of the axon from the site of the lesion. However, the preservation of the endoneural sheath allows the axons to direct their regeneration pedicles towards the originally innervated organ. This type of lesion should have a relatively good prognosis. However, the distance between the site of the lesion and the innervated organ varies. As the axon only regrows distally at an average speed of 1 mm per day, the motor plate and muscle fibers begin to atrophy before an axon reaches them. Finally, Schwann cells in the basement membrane degenerate after prolonged periods and the chances of an axon finding its way diminish for lesions located far from the target organ.<ref>Goldberg G, Goldstein H. AAEM case report 32: nerve injury associated with hip arthroplasty. Muscle Nerve 1998;21:519-27</ref> Time limits thus the potential for reinnervation. If the axon does not reach the motor plaque within two years, the degree of atrophy and scarring of the target muscle becomes so important that restoration of motor function is unlikely.<ref name=":2" />. Moreover, if the motor plate is affected, a sufficient number of axons is required for the muscles to be functional. So there is not always parallelism between electrical and clinical recovery. Indeed, it seems that for an electric reinnervation to be effective, it must be early; otherwise, recovery is still insufficient to restore a function.
 <br />
@@ Line 201: / Line 201: @@
 ==Brachial Plexitis (Parsonage-Turner Syndrome)==
-Brachial plexitis is a condition characterized by acute onset of shoulder pain followed by weakness and/or sensory loss of the shoulder and/or upper extremity. Dreschfeld first described it in 1887. The most important contribution to brachial plexitis was the report of 136 patients by Parsonage and Turner in 1948.<ref>Parsonage MJ, Turner JW. Neuralgic amyotrophy; the shoulder-girdle syndrome. Lancet 1948;1:973-8</ref> The idiopathic form is associated with recent viral infection and vaccination. The hereditary form is an autosomal dominant recurrent brachial plexitis. The incidence is estimated to be approximately 1.64 cases per 100,000 person-years. The disease commonly affects males during their third and seventh decades. The most common initial symptom is acute onset of intense pain around the shoulder followed by weakness. Winged scapula may be observed in 20% of cases (Figure). Thirty percent of the cases are bilateral. Electromyography is a key clue toward the diagnosis. MRI on T2 sequences reveals edema secondary to nerve demyelination. The treatment of brachial plexitis is conservative, based on analgesia and physiotherapeutic rehabilitation.
+Brachial plexitis is a condition characterized by acute onset of shoulder pain followed by weakness and/or sensory loss of the shoulder and/or upper extremity. Dreschfeld first described it in 1887. The most important contribution to brachial plexitis was the report of 136 patients by Parsonage and Turner in 1948.<ref>Parsonage MJ, Turner JW. Neuralgic amyotrophy; the shoulder-girdle syndrome. Lancet 1948;1:973-8</ref> The idiopathic form is associated with recent viral infection and vaccination. The hereditary form is an autosomal dominant recurrent brachial plexitis. The incidence is estimated to be approximately 1.64 cases per 100,000 person-years. The disease commonly affects males during their third and seventh decades. The most common initial symptom is acute onset of intense pain around the shoulder followed by weakness. Winged scapula may be observed in 20% of cases (Figure 2). Thirty percent of the cases are bilateral. Electromyography is a key clue toward the diagnosis. MRI on T2 sequences reveals edema secondary to nerve demyelination. The treatment of brachial plexitis is conservative, based on analgesia and physiotherapeutic rehabilitation.
-<br />[[File:Parsonage Turner Morisod.jpg|thumb|Right winging scapula due to Parsonage-Turner syndrome.]]
+<br />[[File:Parsonage Turner Morisod.jpg|thumb|Figure 2. Right winging scapula due to Parsonage-Turner syndrome.]]
 ==Thoracic Outlet Syndrome==

@@ Line 37: / Line 37: @@
 {| class="wikitable"
 |+Sunderland and Seddon Classifications
-|Sunderland classification
+!Sunderland classification
-|Seddon classification
+!Seddon classification
-|Lesion
+!Lesion
-|Clinical signs
+!Clinical signs
-|Recovery
+!Recovery
 |-
 |Sunderland I

← Older revision		Revision as of 14:47, 16 February 2020
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		+	[[Category:Shoulder]]
	==Bullet Points==		==Bullet Points==
	This subsection does not exist. You can ask for it to be created, but consider checking the search results below to see whether the topic is already covered.		This subsection does not exist. You can ask for it to be created, but consider checking the search results below to see whether the topic is already covered.

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-== Brachial Plexitis (Parsonage-Turner Syndrome) ==
+==Brachial Plexitis (Parsonage-Turner Syndrome)==
 Brachial plexitis is a condition characterized by acute onset of shoulder pain followed by weakness and/or sensory loss of the shoulder and/or upper extremity. Dreschfeld first described it in 1887. The most important contribution to brachial plexitis was the report of 136 patients by Parsonage and Turner in 1948.<ref>Parsonage MJ, Turner JW. Neuralgic amyotrophy; the shoulder-girdle syndrome. Lancet 1948;1:973-8</ref> The idiopathic form is associated with recent viral infection and vaccination. The hereditary form is an autosomal dominant recurrent brachial plexitis. The incidence is estimated to be approximately 1.64 cases per 100,000 person-years. The disease commonly affects males during their third and seventh decades. The most common initial symptom is acute onset of intense pain around the shoulder followed by weakness. Winged scapula may be observed in 20% of cases (Figure). Thirty percent of the cases are bilateral. Electromyography is a key clue toward the diagnosis. MRI on T2 sequences reveals edema secondary to nerve demyelination. The treatment of brachial plexitis is conservative, based on analgesia and physiotherapeutic rehabilitation.
-<br />
+<br />[[File:Parsonage Turner Morisod.jpg|thumb|Right winging scapula due to Parsonage-Turner syndrome.]]
 ==Thoracic Outlet Syndrome==
 The thoracic outlet syndrome is caused by compression of the nerves of the brachial plexus or the vascular bundle in the arm between the first rib, the middle scalene muscle, and the clavicle. In the neurogenic form, the brachial plexus is compressed beneath the scalene muscles or in the costoclavicular space. This syndrome is difficult to diagnose accurately because there is no specific history or physical examination finding. Pain, atrophy, weakness or paresthesias are commonly found.
 <br />
 <br />

@@ Line 200: / Line 200: @@
 == Brachial Plexitis (Parsonage-Turner Syndrome) ==
-Brachial plexitis is a condition characterized by acute onset of shoulder pain followed by weakness and/or sensory loss of the shoulder and/or upper extremity. Dreschfeld first described it in 1887. The most important contribution to brachial plexitis was the report of 136 patients by Parsonage and Turner in 1948.Parsonage MJ, Turner JW. Neuralgic amyotrophy; the shoulder-girdle syndrome. Lancet 1948;1:973-8 The idiopathic form is associated with recent viral infection and vaccination. The hereditary form is an autosomal dominant recurrent brachial plexitis. The incidence is estimated to be approximately 1.64 cases per 100,000 person-years. The disease commonly affects males during their third and seventh decades. The most common initial symptom is acute onset of intense pain around the shoulder followed by weakness. Winged scapula may be observed in 20% of cases (Figure). Thirty percent of the cases are bilateral. Electromyography is a key clue toward the diagnosis. MRI on T2 sequences reveals edema secondary to nerve demyelination. The treatment of brachial plexitis is conservative, based on analgesia and physiotherapeutic rehabilitation.
+Brachial plexitis is a condition characterized by acute onset of shoulder pain followed by weakness and/or sensory loss of the shoulder and/or upper extremity. Dreschfeld first described it in 1887. The most important contribution to brachial plexitis was the report of 136 patients by Parsonage and Turner in 1948.<ref>Parsonage MJ, Turner JW. Neuralgic amyotrophy; the shoulder-girdle syndrome. Lancet 1948;1:973-8</ref> The idiopathic form is associated with recent viral infection and vaccination. The hereditary form is an autosomal dominant recurrent brachial plexitis. The incidence is estimated to be approximately 1.64 cases per 100,000 person-years. The disease commonly affects males during their third and seventh decades. The most common initial symptom is acute onset of intense pain around the shoulder followed by weakness. Winged scapula may be observed in 20% of cases (Figure). Thirty percent of the cases are bilateral. Electromyography is a key clue toward the diagnosis. MRI on T2 sequences reveals edema secondary to nerve demyelination. The treatment of brachial plexitis is conservative, based on analgesia and physiotherapeutic rehabilitation.
 <br />

@@ Line 11: / Line 11: @@
 ==Anatomical Considerations==
-Peripheral nerves are composed of axons, myelin sheaths, connective tissue and blood vessels. A disturbance of nerve function can occur during abnormalities of each of these structures. Each nerve is anatomically divided into individual fascicles, themselves being surrounded by dense connective tissue: the epineurium. The perineurium lies deep in the epineurium. It corresponds to an extension of the pia mater and the arachnoid, functioning as a protective membrane. Endoneurium is an interstitial connective tissue of axons. The internal structure of an axon consists of linear microtubules, essential for axoplasmic flow, and microfilaments. Interruption of this flow causes dysfunction and possibly axonal death with distal degeneration.<ref>Nukada H, Dyck PJ. Acute ischemia causes axonal stasis, swelling, attenuation, and secondary demyelination.Ann Neurol. 1987 Sep;22(3):311-8.</ref><ref>Nuwer M, Schmalzried T, eds. Nerve Palsy: Etiology, Prognosis and Prevention. New York: Churchill Linvingstone; 1991.</ref><ref name=":0">Sunderland S. Nerves and Nerve Injuries. Edinburgh, Churchill Linvingstone 1978.</ref>
+Peripheral nerves are composed of axons, myelin sheaths, connective tissue and blood vessels. A disturbance of nerve function can occur during abnormalities of each of these structures. Each nerve is anatomically divided into individual fascicles, themselves being surrounded by dense connective tissue: the epineurium. The perineurium lies deep in the epineurium. It corresponds to an extension of the pia mater and the arachnoid, functioning as a protective membrane. Endoneurium is an interstitial connective tissue of axons. The internal structure of an axon consists of linear microtubules, essential for axoplasmic flow, and microfilaments. Interruption of this flow causes dysfunction and possibly axonal death with distal degeneration.<ref>Nukada H, Dyck PJ. Acute ischemia causes axonal stasis, swelling, attenuation, and secondary demyelination.Ann Neurol. 1987 Sep;22(3):311-8.</ref><ref name=":2">Nuwer M, Schmalzried T, eds. Nerve Palsy: Etiology, Prognosis and Prevention. New York: Churchill Linvingstone; 1991.</ref><ref name=":0">Sunderland S. Nerves and Nerve Injuries. Edinburgh, Churchill Linvingstone 1978.</ref>
@@ Line 192: / Line 192: @@
 [[File:Diapositive1.jpg|thumb|Recovery of strenght over time after nerve damage]]
-The following explanation may allow to understand the poor functional recovery occasionally observed: in axonotesis, axonal continuity is lost but the structures supporting the nerve are preserved. Axonal degeneration occurs on the distal portion of the axon from the site of the lesion. However, the preservation of the endoneural sheath allows the axons to direct their regeneration pedicles towards the originally innervated organ. This type of lesion should have a relatively good prognosis. However, the distance between the site of the lesion and the innervated organ vary. As the axon only regrows distally at an average speed of 1 mm per day, the motor plate and muscle fibers begin to atrophy before an axon reaches them. Finally, Schwann cells in the basement membrane degenerate after prolonged periods and the chances of an axon finding its way diminish for lesions located far from the target organ.<ref>Goldberg G, Goldstein H. AAEM case report 32: nerve injury associated with hip arthroplasty. Muscle Nerve 1998;21:519-27</ref> Time limits thus the potential for reinnervation. If the axon does not reach the motor plaque within two years, the degree of atrophy and scarring of the target muscle becomes so important that restoration of motor function is unlikely.
+The following explanation may allow to understand the poor functional recovery occasionally observed: in axonotesis, axonal continuity is lost but the structures supporting the nerve are preserved. Axonal degeneration occurs on the distal portion of the axon from the site of the lesion. However, the preservation of the endoneural sheath allows the axons to direct their regeneration pedicles towards the originally innervated organ. This type of lesion should have a relatively good prognosis. However, the distance between the site of the lesion and the innervated organ vary. As the axon only regrows distally at an average speed of 1 mm per day, the motor plate and muscle fibers begin to atrophy before an axon reaches them. Finally, Schwann cells in the basement membrane degenerate after prolonged periods and the chances of an axon finding its way diminish for lesions located far from the target organ.<ref>Goldberg G, Goldstein H. AAEM case report 32: nerve injury associated with hip arthroplasty. Muscle Nerve 1998;21:519-27</ref> Time limits thus the potential for reinnervation. If the axon does not reach the motor plaque within two years, the degree of atrophy and scarring of the target muscle becomes so important that restoration of motor function is unlikely.<ref name=":2" />. Moreover, if the motor plate is affected, a sufficient number of axons is required for the muscles to be functional. So there is not always parallelism between electrical and clinical recovery. Indeed, it seems that for an electric reinnervation to be effective, it must be early; otherwise, recovery is still insufficient to restore a function.
 <br />
@@ Line 199: / Line 199: @@
 <br />

← Older revision		Revision as of 08:09, 16 February 2020
Line 189:		Line 189:

	There are several mechanisms of recovery following motor nerve damage: the resolution of conduction block during neurapraxis, muscle fiber hypertrophy during neuropraxis and axonotesis, intra-muscular collateral reinnervation during partial axonotesis and axonal regeneration from the site of lesion during partial and complete axonotesis and neurotesis.<ref>Robinson LR. Traumatic injury to peripheral nerves. Muscle Nerve 2000;23:863-73</ref>		There are several mechanisms of recovery following motor nerve damage: the resolution of conduction block during neurapraxis, muscle fiber hypertrophy during neuropraxis and axonotesis, intra-muscular collateral reinnervation during partial axonotesis and axonal regeneration from the site of lesion during partial and complete axonotesis and neurotesis.<ref>Robinson LR. Traumatic injury to peripheral nerves. Muscle Nerve 2000;23:863-73</ref>
		+
		+	[[File:Diapositive1.jpg\|thumb\|Recovery of strenght over time after nerve damage]]
		+
		+	The following explanation may allow to understand the poor functional recovery occasionally observed: in axonotesis, axonal continuity is lost but the structures supporting the nerve are preserved. Axonal degeneration occurs on the distal portion of the axon from the site of the lesion. However, the preservation of the endoneural sheath allows the axons to direct their regeneration pedicles towards the originally innervated organ. This type of lesion should have a relatively good prognosis. However, the distance between the site of the lesion and the innervated organ vary. As the axon only regrows distally at an average speed of 1 mm per day, the motor plate and muscle fibers begin to atrophy before an axon reaches them. Finally, Schwann cells in the basement membrane degenerate after prolonged periods and the chances of an axon finding its way diminish for lesions located far from the target organ.<ref>Goldberg G, Goldstein H. AAEM case report 32: nerve injury associated with hip arthroplasty. Muscle Nerve 1998;21:519-27</ref> Time limits thus the potential for reinnervation. If the axon does not reach the motor plaque within two years, the degree of atrophy and scarring of the target muscle becomes so important that restoration of motor function is unlikely.

	<br />		<br />

@@ Line 188: / Line 188: @@
 <br />
-There are several mechanisms of recovery following motor nerve damage: the resolution of conduction block during neurapraxis, muscle fiber hypertrophy during neuropraxis and axonotesis, intra-muscular collateral reinnervation during partial axonotesis and axonal regeneration from the site of lesion during partial and complete axonotesis and neurotesis.Robinson LR. Traumatic injury to peripheral nerves. Muscle Nerve 2000;23:863-73
+There are several mechanisms of recovery following motor nerve damage: the resolution of conduction block during neurapraxis, muscle fiber hypertrophy during neuropraxis and axonotesis, intra-muscular collateral reinnervation during partial axonotesis and axonal regeneration from the site of lesion during partial and complete axonotesis and neurotesis.<ref>Robinson LR. Traumatic injury to peripheral nerves. Muscle Nerve 2000;23:863-73</ref>
 <br />

@@ Line 186: / Line 186: @@
 |1
 |}
 <br />
 ==Clinical Examination==

@@ Line 104: / Line 104: @@
-Sunderland's classification describes well anatomical lesions but does not take into account certain preoperative factors that may influence recovery (such as loss of substance, local ischemia, burns, infections…). Similarly, the age of the patient, the smoking or the delay significantly reduce chance of recovery. A specific scale to predict final prognosis of a nerve injury have been developed.<ref name=":1">Goubier J, Teboul F. Grading of Nerve Injuries. In: Tubbs RS SM, Barbaro N, Rizk E, Loukas M, Spinner RJ., ed. Nerves and Nerve Injuries Pain, Treatment, Injury, Disease and Future Directions: Elsevier 2015:603-10</ref>
+Sunderland's classification describes well anatomical lesions but does not take into account certain preoperative factors that may influence recovery (such as loss of substance, local ischemia, burns, infections…). Similarly, the age of the patient, the smoking or the delay significantly reduce chance of recovery. A specific scale to predict final prognosis of a nerve injury have been developed.<ref name=":1">Goubier J, Teboul F. Grading of Nerve Injuries. In: Tubbs RS SM, Barbaro N, Rizk E, Loukas M, Spinner RJ., ed. Nerves and Nerve Injuries Pain, Treatment, Injury, Disease and Future Directions: Elsevier 2015:603-10</ref> Prognostic scale takes into account the anatomical classification of Sunderland and the most important factors affecting the prognosis of nerve recovery. This scale consists of 15 points. The more points, the poorer the prognosis. A nerve injury scoring 1 point has an excellent prognosis, whereas a lesion with 15 points has a very poor prognosis.
 {| class="wikitable"
@@ Line 129: / Line 129: @@
 |6
 |-
-|'''Type of Injury'''
+| colspan="2" |'''Type of Injury'''
 |-
 |  No associated injuries
@@ Line 141: / Line 140: @@
 |2
 |-
-|'''Delay of motor nerve repair (months)'''
+| colspan="2" |'''Delay of motor nerve repair (months)'''
 |-
 |  < 6
@@ Line 153: / Line 151: @@
 |2
 |-
-|'''Level of motor nerve injury'''
+| colspan="2" |'''Level of motor nerve injury'''
 |-
 |  Distal injury
@@ Line 162: / Line 159: @@
 |1
 |-
-|'''Age of the Patient (years)'''
+| colspan="2" |'''Age of the Patient (years)'''
 |-
 |  Age <20
 |0
 |-
 |  >20 age <50
 |1
 |-
@@ Line 174: / Line 170: @@
 |2
 |-
-|'''Perioperative Smoking'''
+| colspan="2" |'''Perioperative Smoking'''
 |-
 |  No
@@ Line 183: / Line 178: @@
 |1
 |-
-|'''Management in Microsurgical Unit'''
+| colspan="2" |'''Management in Microsurgical Unit'''
 |-
 |  Yes
@@ Line 191: / Line 185: @@
 |  No
 |1
 |}
 <br />