A 16-year-old male with dizziness, parasthesias, and ataxia.

A 16-year-old African-American male with no past medical history presented with gait instability and somnolence. He had intermittent neurological complaints during the prior 4 months, including dizziness, left arm paresthesias, decreased hearing, and inability to control his hands. After an initial diagnosis of vertigo, his symptoms progressed, leading to reevaluation and a second emergency department head computed tomography (CT) scan, which revealed a large area of hypodensity in the cerebellum. Repeat head CT on arrival to the intensive care unit showed a large, left cerebellar hemispheric stroke. This case study discusses the findings of the patient's cerebral angiogram, the diagnosis of fibromuscular dysplasia, and the aggressive treatment that likely prevented further devastating strokes in the brainstem, thalamus, and occipital lobe. This case serves as a reminder that strokes are not just an adult disease and that classic presentations can occur even in unconventional patients.

CXCR2 ligands and G-CSF mediate PKCalpha-induced intraepidermal inflammation.

Transgenic mice overexpressing PKCalpha in the epidermis (K5-PKCalpha mice) exhibit an inducible severe intraepidermal neutrophilic inflammation and systemic neutrophilia when PKCalpha is activated by topical 12-O-tetradecanoylphorbol-13-acetate (TPA). This inducible model of cutaneous inflammation was used to define mediators of skin inflammation that may have clinical relevance. Activation of cutaneous PKCalpha increased the production of the chemotactic factors cytokine-induced neutrophil chemoattractant (KC) and macrophage inflammatory protein 2 (MIP-2) in murine plasma. TPA treatment of cultured K5-PKCalpha keratinocytes also released KC and MIP-2 into culture supernatants through an NF-kappaB-dependent pathway. MIP-2 and KC mediated the infiltration of neutrophils into the epidermis, since this was prevented by ablating CXCR2 in K5-PKCalpha mice or administering neutralizing antibodies against KC or MIP-2. The neutrophilia resulted from PKCalpha-mediated upregulation of cutaneous G-CSF released into the plasma independent of CXCR2. These responses could be inhibited by topical treatment with a PKCalpha-selective inhibitor. Inhibiting PKCalpha also reduced the basal and TNF-alpha- or TPA-induced expression of CXCL8 in cultured psoriatic keratinocytes, suggesting that PKCalpha activity may contribute to psoriatic inflammation. Thus, skin can be the source of circulating factors that have both local and systemic consequences, and these factors, their receptors, and possibly PKCalpha could be therapeutic targets for inhibition of cutaneous inflammation.