Chromhidrosis is a rare condition characterized by the secretion of colored sweat. It is caused by the deposition of lipofuscin in the sweat glands. Cases of red, blue, green, yellow, pink, and black sweat have been reported. Usually, chromhidrosis affects the apocrine glands, mainly on the face and underarms. A limited number of treatment options exist, including regular application of capsaicin cream, and prolonged relief may be provided by botulinum toxin treatment. Chromogenic pigments produced by bacteria (Corynebacterium in particular) are implicated in this condition, but their exact role still requires careful microbiological elucidation. Chromhidrosis of the eccrine glands is rare; it occurs mainly after the ingestion of certain dyes or drugs. See also
List of cutaneous conditions

References
Further reading
Schwarz, T; Neumann, R; Duschet, P; Brückler, B; Klein, W; Oppolzer, G; Bardach, H; Gschnait, F (1989). "Apokrine Chromhidrose" [Apocrine chromhidrosis]. Der Hautarzt (in German). 40 (2): 106–9. PMID 2714985. Marksjr, J (1989). "Treatment of apocrine chromhidrosis with topical capsaicin". Journal of the American Academy of Dermatology. 21 (2 Pt 2): 418–20. doi:10.1016/S0190-9622(89)80050-7. PMID 2474015. Bartels, Eva (2008). "Farbkodierte Dopplersonographie der Vertebralarterien. Vergleich mit der konventionellen Duplexsonographie" [Color coded Doppler sonography of the vertebral arteries. Comparison with conventional duplex sonography]. Ultraschall in der Medizin. 13 (2): 59–66. doi:10.1055/s-2007-1005277. PMID 1604294. == External links ==
Indeed, an ouabain block of Na+-K+ pumps in the cerebellum of a live mouse results in it displaying ataxia and dystonia. Ataxia is observed for lower ouabain concentrations, dystonia is observed at higher ouabain concentrations. A mutation in the Na+-K+ pump (ATP1A3 gene) can cause rapid onset dystonia parkinsonism. The parkinsonism aspect of this disease may be attributable to malfunctioning Na+-K+ pumps in the basal ganglia; the dystonia aspect may be attributable to malfunctioning Na+-K+ pumps in the cerebellum (that act to corrupt its input to the basal ganglia) possibly in Purkinje neurons.Cerebellum issues causing dystonia is described by Filip et al. 2013: "Although dystonia has traditionally been regarded as a basal ganglia dysfunction, recent provocative evidence has emerged of cerebellar involvement in the pathophysiology of this enigmatic disease. It has been suggested that the cerebellum plays an important role in dystonia etiology, from neuroanatomical research of complex networks showing that the cerebellum is connected to a wide range of other central nervous system structures involved in movement control to animal models indicating that signs of dystonia are due to cerebellum dysfunction and completely disappear after cerebellectomy, and finally to clinical observations in secondary dystonia patients with various types of cerebellar lesions. It is proposed that dystonia is a large-scale dysfunction, involving not only cortico-basal ganglia-thalamo-cortical pathways, but the cortico-ponto-cerebello-thalamo-cortical loop as well. Even in the absence of traditional "cerebellar signs" in most dystonia patients, there are more subtle indications of cerebellar dysfunction.