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A Arturo Leis

Publications and source records attributed to A Arturo Leis.

11 recordsLinked to original sources
PubMed2005

Neuromuscular Manifestations of Human West Nile Virus Infection.

Physicians in areas with active West Nile virus (WNV) transmission should be aware that WNV infection can present as a polio-like syndrome and that the spectrum of neuromuscular signs and symptoms may range from acute flaccid paralysis in the absence of fever or meningoencephalitis to subjective weakness and disabling fatigue. This awareness will help to avoid less tenable diagnoses and the morbidity associated with inappropriate treatment. Although anterior horns are the major site of spinal cord pathology, inflammatory changes also may involve spinal sympathetic neurons and ganglia, providing an explanation for the autonomic instability seen in some patients with WNV infection. However, the role that autonomic dysfunction plays in the morbidity and mortality of human WNV infection has to be elucidated. Another unresolved issue with important neuromuscular implications is whether WNV infection may lead to autoimmune disease. Support for this contention arises from reports of WNV patients presenting with various neuromuscular diseases that have a presumed autoimmune mechanism, including Guillain-Barre syndrome, other demyelinating neuropathies, myasthenia gravis, brachial plexopathies, and stiff-person syndrome. Although there is no specific treatment or vaccine currently approved for WNV infection in humans, and the standard is supportive care only, several drugs that can alter the cascade of immunobiochemical events leading to neuronal death may be potentially useful. Among these agents, minocycline (a semisynthetic derivative of tetracycline), interferon alpha, and high-dose corticosteroids are candidate therapies, although human experience is limited. In addition, passive immunization with intravenous immune globulin containing WNV-specific antibodies seems promising, based on anecdotal human reports.

Journal Article↗
PubMed2004

Spinal cord neuropathology in human West Nile virus infection.

CONTEXT: During the 1999 New York City West Nile virus (WNV) outbreak, 4 patients with profound muscle weakness, attributed to Guillain-Barré syndrome, were autopsied. These cases were the first deaths caused by WNV, a flavivirus, to be reported in the United States. The patients' brains had signs of mild viral encephalitis; spinal cords were not examined. During the 2002 national epidemic, several patients in Mississippi had acute flaccid paralysis. Electrophysiologic studies localized the lesions to the anterior horn cells in the spinal gray matter. Four of 193 infected patients in Mississippi died and were autopsied. All 4 experienced muscular weakness and respiratory failure that required intubation. Postmortem examinations focused on the spinal cord. OBJECTIVE: To emphasize apparent tropism of WNV for the ventral gray matter of the spinal cord. DESIGN: Cerebral hemispheres, basal ganglia, diencephalon, brainstem, cerebellum, and spinal cord sections were stained with hematoxylin-eosin and incubated with antibodies to T cells, B cells, and macrophages/microglial cells. RESULTS: We identified neuronophagia, neuronal disappearance, perivascular chronic inflammation, and microglial proliferation in the ventral horns of the spinal cord, especially in the cervical and lumbar segments. Loss of ganglionic neurons, nodules of Nageotte, and perivascular lymphocyte aggregates were found in dorsal root and sympathetic ganglia. Severity of cellular reaction was proportional to the interval length between patient presentation and death. CONCLUSION: West Nile virus caused poliomyelitis. Injury to spinal and sympathetic ganglia mirrored the damage to the spinal gray matter. The disappearance of sympathetic neurons could lead to the autonomic instability observed in some WNV patients, including labile vital signs, hypotension, and potentially lethal cardiac arrhythmias.

Aged↗
PubMed2003

Neurologic manifestations and outcome of West Nile virus infection.

CONTEXT: The neurologic manifestations, laboratory findings, and outcome of patients with West Nile virus (WNV) infection have not been prospectively characterized. OBJECTIVE: To describe prospectively the clinical and laboratory features and long-term outcome of patients with neurologic manifestations of WNV infection. DESIGN, SETTING, AND PARTICIPANTS: From August 1 to September 2, 2002, a community-based, prospective case series was conducted in St Tammany Parish, La. Standardized clinical data were collected on patients with suspected WNV infection. Confirmed WNV-seropositive patients were reassessed at 8 months. MAIN OUTCOME MEASURES: Clinical, neurologic, and laboratory features at initial presentation, and long-term neurologic outcome. RESULTS: Sixteen (37%) of 39 suspected cases had antibodies against WNV; 5 had meningitis, 8 had encephalitis, and 3 had poliomyelitis-like acute flaccid paralysis. Movement disorders, including tremor (15 [94%]), myoclonus (5 [31%]), and parkinsonism (11 [69%]), were common among WNV-seropositive patients. One patient died. At 8-month follow-up, fatigue, headache, and myalgias were persistent symptoms; gait and movement disorders persisted in 6 patients. Patients with WNV meningitis or encephalitis had favorable outcomes, although patients with acute flaccid paralysis did not recover limb strength. CONCLUSIONS: Movement disorders, including tremor, myoclonus, and parkinsonism, may be present during acute illness with WNV infection. Some patients with WNV infection and meningitis or encephalitis ultimately may have good long-term outcome, although an irreversible poliomyelitis-like syndrome may result.

Activities of Daily Living↗
PubMed2003

Depression of spinal motoneurons may underlie weakness associated with severe anemia.

A 37-year-old woman had a 2-week history of progressive weakness, muscle hypotonia, and absent or hypoactive deep tendon reflexes. Nerve conduction studies showed diminished H-reflexes and absent or decreased persistence of F-waves in all limbs. The patient was admitted to the hospital with a diagnosis of Guillain-Barré syndrome. Laboratory studies revealed severe anemia with a hemoglobin level of 4.1 g/dl and hematocrit of 15.1%. Immediate blood transfusion resulted in a hemoglobin of 13.2 g/dl and hematocrit of 40.2%, associated with rapid neurological recovery (normal stretch reflexes and muscle strength) and normalization of F-waves and H-reflexes. This case demonstrates that severe anemia may be associated with signs and symptoms that mimic Guillain-Barré syndrome, both clinically and electrophysiologically. It also suggests that a relative depression of spinal motoneuron excitability may be a possible mechanism for the weakness that is commonly observed in severe anemia.

Adult↗
PubMed2003

Clinical spectrum of muscle weakness in human West Nile virus infection.

Poliomyelitis has recently been identified as a cause of muscle weakness in patients with West Nile virus (WNV) infection. However, the clinical spectrum of WNV-associated weakness has not been described. We reviewed data on 13 patients with WNV infection. Patients with muscle weakness were classified into one of three distinct groups based on clinical features. Group 1 comprised five patients who developed acute flaccid paralysis, four with meningoencephalitis and one without fever or other signs of infection. Paralysis was asymmetric, and involved from one to four limbs in individual patients. Electrodiagnostic studies confirmed involvement of anterior horn cells or motor axons. Group 2 involved two patients without meningoencephalitis who developed severe but reversible muscle weakness that recovered completely within weeks. Muscle weakness involved both lower limbs in one patient and one upper limb in the other. Group 3 consisted of two patients who experienced subjective weakness and disabling fatigue, but had no objective muscle weakness on examination. In addition to the three distinct groups, two other patients developed exaggerated weakness in the distribution of preexisting lower motor neuron dysfunction. We conclude that the clinical spectrum of WNV-associated muscle weakness ranges from acute flaccid paralysis, with or without fever or meningoencephalitis, to disabling fatigue. Also, preexisting dysfunction may predispose anterior horn cells to additional injury from WNV. Awareness of this spectrum will help to avoid erroneous diagnoses and inappropriate treatment.

Acute Disease↗
PubMed2003

Retrograde regeneration following neurotmesis of the ulnar nerve.

A 41-year-old woman experienced a gunshot wound to the forearm with neurotmesis of the ulnar nerve. Surgery 9 months later revealed a neuroma-in-continuity in the midforearm. Intraoperative nerve stimulation failed to elicit direct nerve responses or motor responses from the first dorsal interosseous (FDI) and abductor digiti minimi (ADM) muscles. However, neurotonic discharges in response to mechanical irritation of the neuroma were recorded in the FDI, but not the ADM. Surprisingly, after resecting the ulnar nerve distal to the neuroma, neurotonic discharges were still elicited in the FDI following perturbation of the neuroma. Moreover, neurotonic discharges were elicited during ulnar nerve resection 2 cm proximal to the neuroma. No anastomoses or anomalous branches were noted. The findings suggest that regenerating fibers did not reach the FDI through the distal nerve segment. Rather, we speculate that nerve fibers regenerating at random, or impeded by scar tissue, contacted the proximal nerve portion, at which point growth became polarized in a retrograde direction. Retrograde regeneration may have proceeded to a branch point in the forearm (possibly an undetected anomalous branch or fibrous adhesion), where growth of regenerating fibers extended outward into surrounding damaged tissue planes before redirecting distally to reach the FDI.

Adult↗
PubMed2003

Acute flaccid paralysis and West Nile virus infection.

Acute weakness associated with West Nile virus (WNV) infection has previously been attributed to a peripheral demyelinating process (Guillain-Barré syndrome); however, the exact etiology of this acute flaccid paralysis has not been systematically assessed. To thoroughly describe the clinical, laboratory, and electrodiagnostic features of this paralysis syndrome, we evaluated acute flaccid paralysis that developed in seven patients in the setting of acute WNV infection, consecutively identified in four hospitals in St. Tammany Parish and New Orleans, Louisiana, and Jackson, Mississippi. All patients had acute onset of asymmetric weakness and areflexia but no sensory abnormalities. Clinical and electrodiagnostic data suggested the involvement of spinal anterior horn cells, resulting in a poliomyelitis-like syndrome. In areas in which transmission is occurring, WNV infection should be considered in patients with acute flaccid paralysis. Recognition that such weakness may be of spinal origin may prevent inappropriate treatment and diagnostic testing.

Adult↗