Bilateral Mental Nerve Neuropathy in an Adolescent During Sickle Cell Crises

Hamdoun, Elwaseila; Davis, Lamar; McCrary, Sara Jane; Eklund, Neva Penton; Evans, Owen B.

doi:10.1177/0883073811431498

Cited by 19 publications

(21 citation statements)

References 9 publications

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“…[5][6][7][8][9] Some reports in nonmalignant pediatric cases noted mental nerve neuropathy as a complication in pediatric patients with sickle cell anemia. 10,11 In this case, the lesion of pain and numbness was symmetrical and consistent with bilateral mandibular innervation zone. Hence, it is suspected that the pain and numbness did not arise in the whole mandibular nerve, but in one mental nerve.…”

supporting

confidence: 50%

Chin Numbness and Pain in a Patient with Burkitt Acute Lymphoblastic Leukemia

Sugiyama

Yokoi

Kawakami

et al. 2015

The Journal of Pediatrics

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A 12-year-old boy presented to a primary care dental clinic because of mandibular pain and numbness. Although no dental disorder was revealed, his symptoms were not relieved. He was referred to our hospital on day 5 after onset and was admitted on day 8. His numbness and pain localized around the mandible protuberance and lower lip, and radiated to both ears. No other abnormal physical findings were evident. He underwent brain magnetic resonance imaging (MRI). On MRI scans, some high-intensity areas were detected in the cranial bone on diffusion-weighted images (Figure 1, A). In contrast-enhanced MRI, the mandible bone condyles were enhanced whereas no abnormal finding existed around mental foramen (Figure 1, B) In blood tests, whole white blood cell count was within the normal limits (5300/mm 3 ), but immature leukocytes were observed (myelocytes: 1.0%; metamyelocytes: 0.5%). Serum lactate dehydrogenase level and soluble interleukin-2 receptor concentration were elevated (1322 IU/L and 1170 U/mL, respectively). Serum C-reactive protein level was normal (0.20 mg/dL).The patient received bone marrow puncture on day 15, and blasts (French-American-British classification L3) were seen in bone marrow aspirate (30%) with the karyotype 46, XY. On flow cytometric analysis, CD10, CD19, CD20, CD22, surface IgM, and HLA-DR were positive, and CD5 and CD23 were negative. On fluorescence in situ hybridization analysis, cMyc rearrangement was positive, and IgH/c-Myc translocation and BCL6 rearrangement were negative. Therefore, a diagnosis of Burkitt acute lymphoblastic leukemia (ALL) was made. Blast cells were not detected in the spinal fluid, and progression into Figure 2. Brain MRI after chemotherapy. Residual highintensity areas were seen in the mandible on enhanced MRI.

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supporting

confidence: 50%

Chin Numbness and Pain in a Patient with Burkitt Acute Lymphoblastic Leukemia

Sugiyama

Yokoi

Kawakami

et al. 2015

The Journal of Pediatrics

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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

371

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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“…Se presume que es causada por un infarto del suministro de sangre microvascular del nervio dentario inferior o de sus ramas (19). Por otra parte, se ha reportado que existe una correlación significativa entre la ACF y la necrosis pulpar asintomática en dientes sanos.…”

Section: Etnias (5)unclassified