To the Editor: Seborrheic dermatitis (SD) is characterized by a greasy, scaly eruption in sebaceous-rich areas and is estimated to occur in approximately 3% to 5% of the population.1Gupta A.K. Bluhm B. Seborrheic dermatitis.J Eur Acad Dermatol Venereol. 2004; 18: 13-26Crossref PubMed Scopus (200) Google Scholar Unilateral disease is a rare and unusual presentation.2Bettley F.R. Marten R.H. Unilateral seborrheic dermatitis following a nerve lesion.Arch Dermatol. 1956; 73: 110-115Crossref Scopus (28) Google Scholar The patient was a 44-year-old man who presented to urgent care with neck pain, difficulty with balance, right upper extremity weakness, and 3 to 5 blackout spells per day. Magnetic resonance imaging of the cervical spine revealed tonsillar herniation with Chiari I malformation and syringomyelia extending from the fourth ventricle to T11. Decompression was performed by the neurosurgery service with marked symptomatic improvement. Seven months postoperatively, the patient presented to the dermatology clinic for a greasy, scaly, papulosquamous eruption limited to the right side of his face (Fig 1). Physical examination demonstrated ipsilateral anesthesia in the trigeminal nerve distribution. On further questioning, the patient revealed that the anesthesia and ipsilateral facial eruption began soon after decompression of the Chiari I malformation and syringomyelia. Both the affected and unaffected sides of the face were evaluated by histologic examination of 4-mm punch biopsy specimens from the lateral forehead, culture, and sweat testing. Spongiosis, perifollicular parakeratosis, and superficial perivascular infiltrate was noted on the affected side, consistent with SD. Sebaceous glands demonstrated less differentiation with a thicker germinative layer on the affected side (Fig 2). Neural structures were evaluated by S-100 and Bodian immunohistochemical stains, revealing only one myelinated nerve bundle per tissue cross section (vs 11) in the reticular dermis of the affected side. Cultures revealed coagulase-negative Staphylococcus species on both sides; no Malassezia species was identified. Candida species was present on the lesional side only. Sweat testing was equivalent on both sides using the starch-iodine technique.3Swinehart J.M. Treatment of axillary hyperhidrosis: combination of starch-iodine test with tumescent liposuction techniques.Dermatol Surg. 2000; 26: 392-396Crossref PubMed Scopus (68) Google Scholar Numerous therapies were attempted with only mild to moderate improvement. These included topical corticosteroids, tar shampoo, salicylic acid, antifungal preparations, ketoconazole shampoo, selenium sulfide shampoo, and aggressive debridement. The first case report in the literature of unilateral SD involved a patient with a meningioma encasing the trigeminal nerve that was treated with irradiation.1Gupta A.K. Bluhm B. Seborrheic dermatitis.J Eur Acad Dermatol Venereol. 2004; 18: 13-26Crossref PubMed Scopus (200) Google Scholar Subsequently, the patient developed facial numbness and ipsilateral SD. The affected side demonstrated slight increase in temperature, slight decreased sweating, and slight decreased colony number on the affected side; S albus, S aureus, and Bacillus subtilis were isolated from both sides. Histologic examination was not performed. Interestingly, when the patient's numbness resolved, her SD did as well. Pathogenesis of SD remains unknown, but it is postulated to be multifactorial and involve genetic predisposition, Malassezia species, and dysregulation of immune, sebaceous, and/or neurologic pathways.4Toyoda M. Nakamura M. Morohashi M. Neuropeptides and sebaceous glands.Eur J Dermatol. 2002; 12: 433-437Google Scholar The lack of therapeutic response in our patient is most likely a result of our inability to correct his ipsilateral neurologic deficit. In the original case report, the unilateral SD and ipsilateral numbness resolved concurrently, supporting this hypothesis. This intimate relationship among the genetically predisposed epidermis, sebaceous glands, and milieu (immune, neurologic, micro-organisms) is clearly demonstrated with this unusual presentation of SD. This may also explain why other patients with neurocutaneous disease, such as SD in patients with Parkinson's and HIV, may inadequately respond to conventional therapy. This unusual presentation supports a neurocutaneous mechanism that may involve the sebaceous and immune pathways. Sebaceous differentiation and nerve density has not been reported in patients with Parkinson's and HIV along with SD. A systematic evaluation of these parameters in this unique subset of patients may further elucidate SD multifactorial pathogenesis.