Kaiser Wilhelm syndrome: Obstetric trauma or placental insult in a historical case mimicking Erb’s palsy

Jain, Venu; Sebire, Neil J.; Talbert, D.G.

doi:10.1016/j.mehy.2004.12.027

Cited by 12 publications

(4 citation statements)

References 11 publications

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“…Rather than acting with diplomacy, Kaiser Wilhelm II - leader of Germany and Prussia - engaged in warfare with Serbia, ultimately starting World War I. According to historical records ([1,2] but see [3]), the Kaiser's petulant and outspoken demeanour had foundations laid during childbirth: complications during his breech delivery likely caused injury to his brachial plexus nerves, which led to a permanently limp left arm. His mother, Victoria, favoured her healthier children over her flawed eldest son, which created deep-seated insecurities and bitterness in the future Kaiser.…”

Section: Introductionmentioning

confidence: 99%

Wallerian degeneration: gaining perspective on inflammatory events after peripheral nerve injury

Gaudet

Popovich

Ramer

2011

Journal of Neuroinflammation

690

573

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In this review, we first provide a brief historical perspective, discussing how peripheral nerve injury (PNI) may have caused World War I. We then consider the initiation, progression, and resolution of the cellular inflammatory response after PNI, before comparing the PNI inflammatory response with that induced by spinal cord injury (SCI).In contrast with central nervous system (CNS) axons, those in the periphery have the remarkable ability to regenerate after injury. Nevertheless, peripheral nervous system (PNS) axon regrowth is hampered by nerve gaps created by injury. In addition, the growth-supportive milieu of PNS axons is not sustained over time, precluding long-distance regeneration. Therefore, studying PNI could be instructive for both improving PNS regeneration and recovery after CNS injury. In addition to requiring a robust regenerative response from the injured neuron itself, successful axon regeneration is dependent on the coordinated efforts of non-neuronal cells which release extracellular matrix molecules, cytokines, and growth factors that support axon regrowth. The inflammatory response is initiated by axonal disintegration in the distal nerve stump: this causes blood-nerve barrier permeabilization and activates nearby Schwann cells and resident macrophages via receptors sensitive to tissue damage. Denervated Schwann cells respond to injury by shedding myelin, proliferating, phagocytosing debris, and releasing cytokines that recruit blood-borne monocytes/macrophages. Macrophages take over the bulk of phagocytosis within days of PNI, before exiting the nerve by the circulation once remyelination has occurred. The efficacy of the PNS inflammatory response (although transient) stands in stark contrast with that of the CNS, where the response of nearby cells is associated with inhibitory scar formation, quiescence, and degeneration/apoptosis. Rather than efficiently removing debris before resolving the inflammatory response as in other tissues, macrophages infiltrating the CNS exacerbate cell death and damage by releasing toxic pro-inflammatory mediators over an extended period of time. Future research will help determine how to manipulate PNS and CNS inflammatory responses in order to improve tissue repair and functional recovery.

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Section: Introductionmentioning

confidence: 99%

Wallerian degeneration: gaining perspective on inflammatory events after peripheral nerve injury

Gaudet

Popovich

Ramer

2011

Journal of Neuroinflammation

690

573

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“…Jain et al . showed from a mathematical model that a 50% decrease in placental surface area produces ischaemia of the posteriorly situated left shoulder[ 9 ] Bony causes – Osteomyelitis of the humerus or the cervical vertebrae can present with sudden-onset painful paresis of the upper limb, usually a few days after birth. [ 7 ] Unlike a ‘pseudoparesis’ due to pain, the movements do not recover immediately following resolution of the infection.…”

Section: Discussionmentioning

confidence: 99%

“…Jain et al . showed from a mathematical model that a 50% decrease in placental surface area produces ischaemia of the posteriorly situated left shoulder[ 9 ]…”

Section: Discussionmentioning

confidence: 99%

Birth palsy in congenital varicella syndrome: A lesson in anatomy

Sankaran

Bhardwaj

Venkatramani

et al. 2018

Indian J Plast Surg

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While brachial plexus palsy sustained due to birth trauma is well known, congenital palsies are decidedly rare. We report such a case caused by congenital varicella syndrome, with associated congenital Horner's syndrome and heterochromia iridis. The surprising juxtaposition of a classic upper plexus palsy and a Horner's syndrome raises points of interest. Similar reports in literature are reviewed, and the genesis of a very characteristic group of findings is discussed.

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“…In adults, overall deformities are listed, but the descriptions of sequelar bone lesions are lacking in precision. Moreover, historical cases are sometimes mentioned: King Richard III of England on the strength of his character portrayed by Shakespeare (Rhodes, 1977), but not confirmed thanks to the recent description of his remains (Appleby et al, 2014); or German Emperor Wilhelm II (Jain et al, 2005;Jacoby, 2008).…”

Section: Acquired Forms Of Glenoid Retroversionmentioning

confidence: 99%