There is a new article out that breaks down all of the details of the first 28 patients who got PML while on Tysabri. It is excellent. It tells you things like age of patient, gender, what drugs they took before Tysabri, duration of symptoms before PML was diagnosed, symptoms experienced with PML, whether there were enhancing lesions, duration of first treatment of PML to first symptom of IRIS, symptoms experienced during IRIS, JC viral load in spinal fluid, and status of person at last followup. The article offers many suggestions for trials to be done or further questions to be answered. Interesting facts include 1. 40% of people with PML had enhancing lesions 2. several people had seizures so add that to the list of possible PML symptoms 3. PLEX was used for treatment in all but one case. 4. treatment for IRIS persisted for several months in many cases 5. brain location of lesions is more relevant to prognosis than size of lesions. 6. the survival rate is 71%. 7. 54% received mefloquine and 39% received mirtazapine as adjunctive treatment along with PLEX and steroids. 8. 3 out of the 28 were treatment naive before Tysabri 9. 7 out of the 8 deaths were in the USA

"Natalizumab-associated progressive multifocal leukoencephalopathy in patients with multiple sclerosis: lessons from 28 cases," The Lancet Neurology, Volume 9, Issue 4, Pages 425 - 437, April 2010

Here is the abstract:

Background Treatment of multiple sclerosis with natalizumab is complicated by rare occurrence of progressive
multifocal leukoencephalopathy (PML). Between July, 2006, and November, 2009, there were 28 cases of confi rmed
PML in patients with multiple sclerosis treated with natalizumab. Assessment of these clinical cases will help to
inform future therapeutic judgments and improve the outcomes for patients.
Recent developments The risk of PML increases with duration of exposure to natalizumab over the fi rst 3 years of
treatment. No new cases occurred during the fi rst two years of natalizumab marketing but, by the end of November,
2009, 28 cases had been confi rmed, of which eight were fatal. The median treatment duration to onset of symptoms
was 25 months (range 6–80 months). The presenting symptoms most commonly included changes in cognition,
personality, and motor performance, but several cases had seizures as the fi rst clinical event. Although PML has
developed in patients without any previous use of disease-modifying therapies for multiple sclerosis, previous therapy
with immunosuppressants might increase risk. Clinical diagnosis by use of MRI and detection of JC virus in the CSF
was established in all but one case. Management of PML has routinely used plasma exchange (PLEX) or
immunoabsorption to hasten clearance of natalizumab and shorten the period in which natalizumab remains active
(usually several months). Exacerbation of symptoms and enlargement of lesions on MRI have occurred within a few
days to a few weeks after PLEX, indicative of immune reconstitution infl ammatory syndrome (IRIS). This syndrome
seems to be more common and more severe in patients with natalizumab-associated PML than it is in patients with
HIV-associated PML.
Where next? Diagnosis of natalizumab-associated PML requires optimised clinical vigilance, reliable and sensitive
PCR testing of the JC virus, and broadened criteria for recognition of PML lesions by use of MRI, including contrast
enhancement. Optimising the management of IRIS reactions will be needed to improve outcomes. Predictive markers
for patients at risk for PML must be sought. It is crucial to monitor the risk incurred during use of natalizumab
beyond 3 years.