one was still undergoing rehabilitation. The five patients with WNM functioned at normal or nearly normal levels, according to the results of Barthel and modified Rankin scoring systems. Five patients with severe WNE also had recovered premorbid levels of functioning without residual disability; two WNE patients relied on walkers.
The three patients with AFP were faring poorly 8 months after onset. All continued to experience profound muscle weakness; they required wheelchairs and had difficulty in accomplishing such daily activities as grooming and housekeeping. Clinical findings and electrodiagnostic data on two of them suggested a poliomyelitis-like syndrome with involvement of anterior horn cells of the spinal cord. Electromyographic data suggested chronic denervation and permanent loss of motor axons in affected limbs.
A number of studies have been conducted to elucidate the outcomes of patients infected with West Nile virus who develop focal neurologic deficits, especially AFP. Saad and colleagues (2005) reviewed all cases of AFP related to WNV reported in the English-language literature from January 1999 to March 2004 whose clinical characteristics were described in sufficient detail (53 subjects, including the three described above); they added three cases of their own. Forty of the 56 subjects survived the acute phase of disease had a known long-term health outcome. All 40 suffered some degree of persistent neurologic impairment or weakness at the time of long-term followup. As a case in point, the authors noted a survivor who remained quadriplegic and ventilator-dependent after 20 months of followup.
In cases of WNV-induced focal neurologic deficits, the rate and degree of recovery of muscle strength appears to vary by limb and patient; the initial severity of paralysis may not predict the final outcome (Cao et al. 2005). Cao and colleagues reached those conclusions by measuring the muscle strength and overall motor function of 11 subjects for 6-21 months after the onset of AFP. A 36-year-old woman paralyzed in one leg recovered minimal strength during the 21-month period. In contrast, a 44-year-old man with severe four-limb paralysis who was hospitalized for respiratory distress started to walk within 1 month and recovered full strength in all limbs after 9 months (with decreased endurance). Between those extremes, a third patient became paralyzed to various degrees in four limbs and was partially recovered at 21 months. A small case-control study suggested a correlation between the estimated numbers of surviving motor units in a muscle and the degree of improvement of muscle strength (Cao et al. 2005).
Neurophysiologic, radiologic, and pathologic studies in humans and animals indicate that the underlying mechanism of WNV AFP is damage to the anterior horn cells of the spinal cord akin to the damage caused by poliomyelitis virus (Saad et al. 2005). That suggests that most patients with WNV AFP will not recover completely.
As Klee et al. (2004) noted, WNV infection is clinically similar to St. Louis encephalitis. Patients with the latter disease have reported disability up to 5 years after the acute illness. Persistent symptoms of St. Louis encephalitis have included fatigue, headache, nervousness, inability to concentrate, depression, and problems with gait and balance throughout the convalescent period of 6 months to 3 years.
The committee concludes that there is sufficient evidence of an association between acute West Nile virus infection and variable levels of physical, functional, or cognitive disability that may persist for months, years, or permanently.