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.
Tipranavir (TPV), or tipranavir disodium, is a nonpeptidic protease inhibitor (PI) manufactured by Boehringer Ingelheim under the trade name Aptivus  AP-tiv-əs. It is administered with ritonavir in combination therapy to treat HIV infection. Tipranavir has the ability to inhibit the replication of viruses that are resistant to other protease inhibitors and it recommended for patients who are resistant to other treatments. Resistance to tipranavir itself seems to require multiple mutations. Tipranavir was approved by the Food and Drug Administration (FDA) on June 22, 2005, and was approved for pediatric use on June 24, 2008.Tipranavir should only be taken in combination with ritonavir and other antiretroviral drugs, and is not approved for treatment-naïve patients. Like lopinavir and atazanavir, it is very potent and is effective in salvage therapy for patients with drug resistance. However, side effects of tipranavir may be more severe than those of other antiretrovirals. Some side effects include intracranial hemorrhage, hepatitis, hepatic decompensation, hyperglycemia and diabetes mellitus. The drug has also been shown to cause increases in total cholesterol and triglycerides.Aptivus labeling has a black box warning regarding hepatotoxicity and intracranial hemorrhage. References
External links
"Tipranavir". Drug Information Portal. U.S. National Library of Medicine.