SAVANNAH, GA. — Any patient who presents with the neurologic symptoms of acute-onset weakness or paralysis during mosquito season should be evaluated for West Nile virus infection, regardless of whether there was a viral prodrome.
Only about 1% of West Nile patients develop symptoms, but about 21% of that group develop a neurologic complication. Recovery is highly variable and almost impossible to predict, two researchers said at the annual meeting of the American Association of Electrodiagnostic Medicine.
An early and virulent season for West Nile virus infection has been predicted for California and the southwestern United States by the Centers for Disease Control and Prevention's division of vector-borne infectious diseases. The culprit: a wetter-than-normal winter.
The International Society for Infectious Diseases has predicted a tough year for Oregon in terms of West Nile virus infection. The state saw 88 deaths from West Nile in 2004, according to CDC data. State public health officials are meeting to develop control strategies (www.promedmail.org/pls/pm/pm?an=20050305.0670
“These paralytic illnesses are seen a lot in patients who are elderly, immunocompromised, or otherwise sick, but every once in a while you'll see them in a young, healthy patient,” said Bjorn Oskarsson, M.D.
“Severity of illness at onset isn't a good predictor of recovery,” noted Dr. Oskarsson, a neurologic fellow at the University of Colorado, Denver.
Weakness or paralysis associated with West Nile infection apparently occurs when the virus destroys motor neurons in the anterior horn of the spinal cord. Magnetic resonance imaging is generally unhelpful in symptomatic infection, but patients with paralytic illness often show abnormal signal intensity in the anterior horn, he said in a poster presentation.
Jun Li, M.D., said needle electromyography shows severe denervation in the muscles of weak limbs and their corresponding paraspinal muscles. The findings confirm the localization of the lesion to the anterior horn motor neurons or their ventral nerve roots.
“The cardinal clinical feature of these patients is acute asymmetric flaccid paralysis that reaches a plateau within hours in most patients,” said Dr. Li of the department of neurology at Wayne State University, Detroit. The paralysis is slightly more frequent in the lower extremities than in the upper, and there little or no sensory disturbance.
Many patients report a flu-like illness preceding onset of weakness by days or weeks, but this is not a certainty. Paralysis can occur in previously healthy individuals as well as those who are immunocompromised or those with chronic health problems.
West Nile virus has become endemic in most states, so the presence of IgM antibodies in serum is no longer an acceptable way of confirming the diagnosis, Dr. Li noted. Instead, the antibodies must be detected in cerebrospinal fluid by enzyme-linked immunosorbent assay.
Patients with a paralytic complication may also show increased serum creatine kinase, ranging from several hundred up to 20,000 mg/dL. “This elevated CK may have originated from necrotized muscle fibers,” Dr. Li said.
There is no current treatment for the condition, he noted. Intravenous immunoglobulin has been found ineffective.
Both Dr. Li and Dr. Oskarsson presented case studies illustrating the unpredictable nature of this illness.
Dr. Li presented two cases. A previously healthy 36-year-old woman developed a mild flu-like illness followed by low back pain. She then awoke to find her left leg paralyzed. She was unresponsive to a short course of intravenous immunoglobulin.
The second case was a previously healthy 44-year-old man who first noticed a tingling sensation in his back followed by a flu-like illness. Four days later, his legs suddenly became paralyzed. Ten days later, his right arm was paralyzed and within another 24 hours, the left arm was also paralyzed. He also developed bilateral facial muscle weakness.
These two patients illustrate the unpredictable outcomes of this illness, Dr. Li noted. The man had more systemic symptoms and severe four-limb paralysis. His condition appeared much worse than that of the woman. Yet his strength recovered completely, while the woman's leg paralysis improved only minimally after 20 months.
Dr. Oskarsson presented five cases; three involved immunocompromise.
One patient died. She was a 46-year-old woman with a history of bone marrow transplant for large cell lymphoma. She presented with generalized weakness after a flu-like illness. She rapidly became comatose. Her brain MRI showed severe panencephalitic changes with multifocal necrosis in the cerebral deep gray nuclei, brainstem, and spinal cord.
The other patients survived, but only one regained baseline strength: a 48-year old woman with a prior kidney transplant. A month after developing gastroenteritis she became confused and developed proximal bilateral arm weakness.