Neuro-Sweet's disease

Maxwell, Gemma; Archibald, Neil; Turnbull, Doug M.

doi:10.1136/practneurol-2011-000067

Cited by 11 publications

(9 citation statements)

References 7 publications

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“…Neurologic involvement in Sweet syndrome is uncommon and likely underreported. In a review of Sweet syndrome with neurologic manifestations, the most common presenting symptoms were headaches, seizures, and disturbance of consciousness [11,12]. Normal brain CT or MRI was found in 27% of patients and CSF sampling commonly reveal an increased cell count with lymphocytosis as well as increased CSF protein [11].…”

Section: Discussionmentioning

confidence: 99%

Sweet syndrome with panniculitis, arthralgia, episcleritis, and neurologic involvement precipitated by antibiotics

Kwok¹,

Mahmood²,

Salopek

2014

Dermatology Online Journal

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Background: Sweet syndrome is an uncommon skin condition, often idiopathic in origin although it may be reactive to various systemic conditions, recent infections, underlying malignancies, and medications.Objective & Method: To present a case highlighting a rare clinical presentation and to review the causes of Sweet syndrome with an emphasis on drug-induced etiologies. Results:We describe a 45-year-old woman who developed Sweet syndrome while receiving nitrofurantoin and ciprofloxacin for a urinary tract infection. Her course of disease was complicated by arthralgias, episcleritis, headaches, and erythema nodosum-like subcutaneous involvement. There was marked improvement with discontinuation of the inciting antibiotics and initiation of systemic steroids. Conclusion:This case illustrates Sweet syndrome related to nitrofurantoin and/or ciprofloxacin. This is the second report of Sweet syndrome related to these antibiotics and the first associated with ocular, joint, and neurologic involvement.

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Section: Discussionmentioning

confidence: 99%

Sweet syndrome with panniculitis, arthralgia, episcleritis, and neurologic involvement precipitated by antibiotics

Kwok¹,

Mahmood²,

Salopek

2014

Dermatology Online Journal

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“…Zudem können zahlreiche Medikamente, v. a. der Granulozyten-koloniestimulierende Faktor (GCSF), ein Sweet-Syndrom auslösen. Der Erkrankung geht oft eine 1-3 Wochen zuvor aufgetretene bakterielle Infektion voraus [8]. Neben der Affektion der Haut kann es auch zu anderen Organmanifestationen (Augen, Lunge, Leber, Nieren, Gastrointestinaltrakt, Knochenmark, Muskeln und ZNS) kommen [7].…”

Section: Diskussionunclassified

Papeln und Kopfschmerz – wie passt das zusammen?

et al. 2020

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Papeln und Kopfschmerz-wie passt das zusammen? Anamnese Eine 42-jährige osteuropäische Patientin stellte sich aufgrund von seit 2 Tagen bestehenden Kopfschmerzen drückenden Charakters und hoher Intensität vor, die sie als beidseits vom Nacken aus über den Hinterkopf nach frontal ausstrahlend beschrieb. Eine symptomatische Therapie erbrachte keinen Erfolg. Zudem bestand seit 3 Tagen ein Exanthem an den Armen und am Dekolleté. Im Monat zuvor habe sie einen Insektenstich am Unterschenkel gehabt, der sich infiziert habe und mit einer Lymphknotenschwellung einhergegangen sei. Ambulant sei eine antibiotische Therapie mit Amoxicillin über 5 Tage durchgeführt worden. Seit dem Vortag der Aufnahme habe sie Fieber bis 39,1°C. Seit 3 Wochen leide sie an Husten, den sie auf einen bekannten Heuschnupfen zurückführe.

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“…The MRI abnormalities in NBD have a predilection for the brainstem and deep gray nuclei. [2][3][4] Importantly, steroids, which are extremely effective in NSD, can aggravate mucocutaneous lesions in NBD. 2,3 NSD attacks may recur with steroid discontinuation.…”

Section: Practical Implicationsmentioning

confidence: 99%

“…[2][3][4] Importantly, steroids, which are extremely effective in NSD, can aggravate mucocutaneous lesions in NBD. 2,3 NSD attacks may recur with steroid discontinuation. Other therapies used for Sweet syndrome include topical steroids, dapsone, cyclosporine, and colchicine, but there are no established therapies beyond corticosteroids for NSD.…”

Section: Practical Implicationsmentioning

confidence: 99%

“…2 Brain MRI can be normal or include T2 hyperintensities in cortical or subcortical regions (without site predilection), often with asymmetries, and meningeal enhancement/thickening may also be present. 3 Proposed diagnostic criteria for probable NSD stipulate that neurologic symptoms respond to steroids and that tender erythematous plaques with pathology characteristic of Sweet syndrome are found on skin biopsy (criteria fulfilled by our patient).…”

Section: Practical Implicationsmentioning

confidence: 99%

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Neuro-Sweet disease

et al. 2016

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N euro-Sweet disease (NSD) should be considered in the differential diagnosis of recurrent aseptic meningoencephalitis; a thorough skin examination and early skin biopsy can facilitate diagnosis and early treatment for this steroidresponsive condition. Case reportA 49-year-old African American woman developed acute confusion followed by speech arrest, right face and arm weakness, and hemineglect that spontaneously resolved 1 hour from onset. Brain MRI showed fluid-attenuated inversion recovery (FLAIR) hyperintensities and cortical thickening in bilateral cingulate gyri and left insular and frontal cortex (figure 1, A and B). Her examination showed a Montreal Cognitive Assessment (MoCA) score of 8/30. CSF showed 327 nucleated cells/mL (lymphocyte predominant) and protein 120 mg/dL. Erythrocyte sedimentation rate (ESR) was 36 mm/h, C-reactive protein (CRP) 5.3 mg/L, peripheral leukocyte count 14.3 K/mm 3 with 67% neutrophils. No infectious etiology was identified. Pertinent negatives included the following: CSF and serum paraneoplastic panel; CSF herpes simplex virus, cytomegalovirus, and varicella-zoster virus PCRs, and West Nile virus immunoglobulin M; CSF and serum protein electrophoresis; and serum thyroidstimulating hormone, TPO antibody, HIV, rapid plasma reagin, antinuclear antibodies, extractable nuclear antigen, and antineutrophil cytoplasmic antibodies. CSF cytology and body PET/CT demonstrated no malignancy. EEG showed left hemispheric slowing. Levetiracetam was started given the presenting transient deficits. After 5 g of IV methylprednisolone (empiric treatment for presumed autoimmune encephalitis), she was discharged on oral prednisone with an improved MoCA score of 18.The patient was readmitted 11 days later with transient confusion and fevers to 39.5°C after errantly tapering her prednisone off within 1 week of discharge. A 1 cm erythematous papule was noted above her lip. A repeat EEG was normal; repeat brain MRI and CSF analysis showed interval improvement. Oral prednisone was restarted. In clinic on the last day of her planned steroid taper, she was doing well, but memory, language, and executive dysfunction persisted (MoCA 16). Brain MRI showed resolution of the FLAIR changes (figure 1, C and D). Her skin lesion had disappeared. Because of a mild headache and depressed mood, venlafaxine was started.A week later, the patient re-presented with a temperature of 39.1°C and no identifiable infectious etiology; however, tender, edematous violaceous papules had erupted over all her limbs and abdomen (figure 2, A and B). Her neurologic examination was unchanged. Venlafaxine was stopped with concern for a drug allergy. ESR was 73 mm/h. A skin biopsy revealed dermal neutrophilic infiltration and septal panniculitis without vasculitis, diagnostic of Sweet syndrome (figure 2, C and D). The rash cleared with Practical ImplicationsNeuro-Sweet disease should be considered in the differential diagnosis of recurrent aseptic meningoencephalitis; a thorough skin examination and early skin biopsy can facilitate di...

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Neuro-Sweet's disease

Cited by 11 publications

References 7 publications

Sweet syndrome with panniculitis, arthralgia, episcleritis, and neurologic involvement precipitated by antibiotics

Sweet syndrome with panniculitis, arthralgia, episcleritis, and neurologic involvement precipitated by antibiotics

Papeln und Kopfschmerz – wie passt das zusammen?

Neuro-Sweet disease

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