Mental nerve paresthesia secondary to sickle-cell crisis

Kirson, Lyle E.; Tomaro, Anthony J.

doi:10.1016/0030-4220(79)90295-0

Cited by 34 publications

(20 citation statements)

References 14 publications

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“…Anecdotally, neuropathic pain in SCD may be the result of tissue damage after vaso-occlusion of blood vessels of nerves (vasa vasorum). These include mental nerve neuropathy, [85][86][87][88] trigeminal neuralgia, 89 acute proximal median mononeuropathy, 90 entrapment neuropathy, 91 acute demyelinating polyneuropathy, 91 ischemic optic neuropathy, 92 orbital infarction, 93 orbital apex syndrome, 94 and spinal cord infarction. 95 Among the peripheral neuropathic pain syndromes in SCD, mental nerve neuropathy was the most commonly reported.…”

Section: Neuropathic Painmentioning

confidence: 99%

Sickle cell pain: a critical reappraisal

Ballas

Gupta

Adams-Graves

2012

Blood

358

427

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Sickle cell pain includes 3 types: acute recurrent painful crises, chronic pain syndromes, and neuropathic pain. The acute painful crisis is the hallmark of the disease and the most common cause of hospitalization and treatment in the emergency department. It evolves through 4 phases: prodromal, initial, established, and resolving. Each acute painful episode is associated with inflammation that worsens with recurrent episodes, often culminating in serious complications and organ damage, such as acute chest syndrome, multiorgan failure, and sudden death. Three pathophysiologic events operate in unison during the prodromal phase of the crisis: vaso-occlusion, inflammation, and nociception. Aborting the acute painful episode at the prodromal phase could potentially prevent or minimize tissue damage. Our hypothesis is that managing these events with hydration, anti-inflammatory drugs, aggressive analgesia, and possibly vasodilators could abort the crisis and prevent or minimize further damage. Chronic pain syndromes are associated with or accompany avascular necrosis and leg ulcers. Neuropathic pain is not well studied in patients with sickle cell disease but has been modeled in the transgenic sickle mouse. Management of sickle cell pain should be based on its own pathophysiologic mechanisms rather than borrowing guidelines from other nonsickle pain syndromes. (Blood. 2012;120(18): 3647-3656) IntroductionSickle cell disease (SCD) has been primarily considered a disease of children with a few patients surviving to adulthood. Between 1910 and 1950, the median survival of patients with SCD was Ͻ 20 years of age. 1 Sudden death occurred in ϳ 41% of the patients, whereas 29% deaths occurred within 24 hours after the onset of painful crises. 2 By 1980, 50% of children survived to 20 years of age; and by 2009, survival to age 20 years increased to 85% of children. 2 However, if we rewind the clock by more than a century when SCD was first described in the United States, we find that the first 4 SCD patients reported were adults with leg ulcers. [3][4][5][6] Before 1910, there were observations among adult African slaves suggestive of SCD with immunity to malaria and high prevalence of leg ulcers. 7 Moreover, autopsy on a slave with history of fever and respiratory illness in 1846 showed absence of the spleen. 8 The inevitable question then is: where were the children with SCD in the United States before 1910? There must have been children with SCD. The patient reported by Cook and Meyer 5 gave family history of brothers and sisters who died in early life of a disease associated with grave anemia. These children must have lived, suffered, and died prematurely, the dark side of the discovery of sickle cell anemia in the United States. 9 It was not until the early 1930s that children with SCD were recognized. Sickle cell pain between 1930 and 1960Between 1930 and 1960, the emphasis was on studying the basic science of SCD. This period witnessed quantum leaps in defining the specific molecular signature of SCD with the advent ...

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Section: Neuropathic Painmentioning

confidence: 99%

Sickle cell pain: a critical reappraisal

Ballas

Gupta

Adams-Graves

2012

Blood

358

427

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“…There have been reports of paresthesia of the mental nerve secondary to sickle‐cell anemia crises (Kirson and Tomaro, 1979; Friedlander et al , 1980), benign lymphogranulomatosis (sarcoidosis) (Cohen and Reinhardt, 1982), amyloidosis (Spillane and Wells, 1959; Gastaut and Michel, 1984), diabetic polyradiculoneuropathy (Casamassimo and Tuker, 1988), and multiple scleroses – such paresthesias being the first symptom or manifestation of the disease in 2–3% of patients (Roistacher, 1973; Durward et al , 1990). Likewise, alterations of the mental nerve have been described in located forms of Castelman's disease (Gabrielli et al , 1991), poisoning by trichloroethylene or stilbamidine (Goldstein et al , 1963), and cerebrovascular diseases such as spontaneous bleeding of the protuberance (Berlit, 1989) or ischemic vertebrobasilar damage (Nelson et al , 1986).…”

Section: Trigeminal Neuropathy Variantsmentioning

confidence: 99%

Trigeminal neuropathy

Peñarrocha

Marti³

et al. 2007

Oral Diseases

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Trigeminal neuropathies (TNs) are well recognized disorders characterized and manifesting as skin and mucosal numbness in the region innervated by the trigeminal nerve. Facial numbness indicates trigeminal sensory alteration affecting the trigeminal system. TNs always pose differential location difficulties as multiple diseases are capable of producing them: they can be the result of traumatism, tumors, or diseases of the connective tissue, infectious or demyelinating diseases, or may be of idiopathic origin. Their importance is explained by the fact that TN may represent the first manifestation of tumor disease, or of relapse in patients with prior neoplastic processes. As such, these manifestations are ominous, and patient life expectancy is often short. The clinical exploration reveals a loss of sensitivity in the cutaneous territory corresponding to the affected nerve, which can be partial (hypoesthesia) or complete (anesthesia). The sensory defect is occasionally associated with hyperesthesia (i.e., the patient suffers a decrease in sensory perception, but when sensation is perceived, it may cause considerable discomfort). Complementary studies are needed to establish the etiologic diagnosis, with laboratory tests to discard the possible causative diseases underlying the trigeminal neuropathy, and the opportune radiographic examinations in the form of plain X‐rays or a routine cranial computed tomography scan.

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“…The first is tissue damage secondary to occlusion of blood vessels that supply the nerves as can be found in mental nerve neuropathy and spinal cord infarction. [290][291][292] The second seems to be chronic pain. Persistent chronic pain, the resulting inflammation, and/or pain management seem to lead to neuropathic pain.…”

Section: Introductionmentioning

confidence: 99%