A young adult with leptospirosis associated acute inflammatory demyelinating polyneuropathy (original) (raw)
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Acta Neurol …, 2010
Atypical acute inflammatory demyelinating polyneuropathy in the setting of HIV infection: Report of two cases RESUMEN La polineuropatia desmielinizante aguda (AIDP) es un desorden inmune que afecta el nervio periférico produciendo lesión axonal o mielínica. las infecciones respiratorias altas, gastrointestinales o los cuadros febriles inespecíficos usualmente preceden este caudro clínico caracterizado por debilidad progresiva y disminución de reflejos miotendinosos. En el paciente con infección VIH la AIDP usulamnete aparece en el periodo de seroconversión cuando el conteo de CD4 es mayor a 500 células/uL. Se presume origen infecciosos a pesar de no existir un anticuerpo específico. reportamos dos casos de paciente con VIH y ADPI con presentación atípica. El primero con un conteo de CD4 menos a 100 células/uL, el segundo en el contexto de síndrome de reconstitución inmunológica (IRIS). Ambos pacientes tuvieron recuperación satisfactoria luego de tratamiento con inmunoglobulina intravenosa y suspensión temporal del tratamiento antiretroviral respectivamente. PALABRAS CLAVES. Síndrome de inmunodeficiencia adquirida, Polineuropatias.
A 46-year-old man with Fever and numbness of limbs
Tanaffos, 2011
A 46 year-old man was referred to this center with low grade fever and gradual progressive numbness of lower extremities since 4 months ago. He reported loss of superficial sensation of the distal aspect of the left foot started 4 months ago; it then extended to the right side and also both hands. He had no other symptoms or abnormal findings in recent months. Primary evaluations including laboratory analysis and imaging studies were unremarkable. He was a dentist, married, with three children, non-smoker and with no habitual history. His past medical history was insignificant with no history of recent travelling, exposure or transfusion. On admission, he looked well. Physical examination revealed low grade fever, pallor and loss of superficial sensation in feet and hands with no other significant findings. Laboratory analysis showed 11,000/mm3 white blood cells, 10 gr/dl hemoglobin and 300,000/mm3 platelet count, 80 mm/hr erythrocyte sedimentation rate with normal liver function tests, coagulation profile, serum lactate dehydrogenase, urinalysis, blood urea and creatinine concentrations. Angiotensin converting enzyme (ACE), antinuclear antibody (ANA), antineutrophil cytoplasmic antibodies (ANCA), serum protein electrophoresis and cerebrospinal fluid analysis were all normal. Brain and neck magnetic resonance imaging (MRI) were unremarkable. Electromyography and NCV study (EMG-NCV) were repeated because of gradual development of motor dysfunction when grasping and standing during admission and revealed severe motor nerve dysfunction. Chest x-ray showed reticular pattern in upper and lower lobes of the right lung. Chest computed tomography of the patient is shown in . Scan of paranasal sinuses showed right maxillary sinusitis. Bronchoscopy was performed to evaluate lung lesions. A nodular endobronchial lesion was seen in right main bronchus. Histopathologic examination was non-specific and non-diagnostic. Following admission, multiple macular reddish lesions appeared on legs. Dermal biopsy showed perivascular infiltration. Finally a diagnostic procedure was performed. (Tanaffos 2011; 10(2): 75-78) . Chest x-ray and high resolusion computed tomography of the chest.
Case 7-2010: A 49-Year-Old Man with Peripheral Neuropathy and Ascites
Pr e sen tat ion of C a se Dr. Caron A. Jacobson (Medical Oncology): A 49-year-old man was admitted to this hospital because of ascites. The patient had been well until approximately 4 years earlier, when paresthesias of both feet, weakness of the lower legs, and bilateral foot drop developed gradually. Three years before admission, he saw a neurologist at another hospital. Laboratory test results, including testing for autoantibodies, were reportedly normal. Electromyography (EMG) reportedly showed prolonged F responses in both feet, normal motor and sensory responses in the distal segments of the arms, and no motor responses in the intrinsic foot muscles. A diagnosis of chronic inflamma-tory demyelinating polyneuropathy (CIDP) was made, and therapy with intravenous immune globulin was begun. Two and a half years before admission, the patient was referred to the neurol-ogy clinic of this hospital. On examination, the Romberg test was markedly abnormal ; there was bilateral foot drop, and the patient was unable to walk on his toes or heels. He was able to sign his name but not without visual control. Strength (on a scale of 0 to 5, where 5 is normal) in the ankle dorsiflexors measured 1 to 2; in the muscles of ankle eversion and inversion, 4−; in the extensor hallucis longus, extensor digitorum brevis, and toe flexors, 0; and in the plantar flexors, 4− to 4. The left hand was mildly weak, particularly the abductor pollicis brevis, and strength was normal in the proximal arms. Deep-tendon reflexes were absent. Perception of vibration was absent in both first toes, decreased in both ankles, and normal at the knees and fingers. Position sense was diminished in both first toes. There was no muscle atrophy or fasciculation, and the remainder of the neurologic examination was normal. As compared with the previous study, EMG and nerve-conduction studies showed decreased sensory responses, absent sural-nerve responses, prolonged F-wave latencies, and more prominent denerva-tion in the tibialis anterior and medial gastrocnemius muscles, features consistent with a demyelinating polyneuropathy. During the next 6 months, weakness in the patient's legs and arms increased, and intermittent stabbing pain in the lower legs developed. Intravenous immune
A Rare Case of HIV-Induced Inflammatory Demyelinating Polyneuropathy
American Journal of Medical Case Reports, 2020
Background: Acute inflammatory demyelinating polyneuropathy (AIDP) is an uncommon form of neuropathy in HIV-infected patients that can cause pain, sensory disturbance, and motor weakness. Case presentation: A 23-year-old African American male with past medical history of Guillain-Barre Syndrome (GBS), Lyme disease, and sexually transmitted infections including syphilis and chlamydia presented with acute back pain radiating to bilateral lower extremities with worsening right foot weakness for four days. Cerebrospinal fluid (CSF) studies including meningoencephalitis panel were negative as well as blood tests for Lyme disease and HIV antibody testing. Patient was initially treated with penicillin for positive treponemal serology but without improvement in lower extremity weakness. Electromyogram showed evidence of early demyelinating motor polyneuropathy. Four days after presentation, repeat HIV antibody testing returned positive. Recurrent AIDP in this case was suspected to be secondary to acute HIV infection, and highly active antiretroviral therapy (HAART) was administered along with intravenous immunoglobulin (IVIG). Muscle strength improved with therapy and patient was expected to have continued improvement with intensive rehabilitation after discharge. Conclusion: Acute inflammatory demyelinating polyneuropathy (AIDP) tends to present early in course of HIV infection. Therefore, HIV testing should be obtained in individuals presenting with new neurological deficits. Our patient received HAART therapy, in addition to the traditional modalities to manage AIDP, which led to a substantial recovery of his sensorimotor function.