Absinthe, the nervous system and painting.
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Biomedical subjects
Publications and source records attributed to Tiina Rekand.
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BACKGROUND: Postpolio syndrome is characterised by new muscular weakness, pain, and fatigue several decades after the acute polio, and affects approximately 1/4 of patients with previous paralytic polio. MATERIAL AND METHODS: A 47-year-old woman with a previous history of acute poliomyelitis developed progressive muscular weakness in her left arm and right leg with muscular pain and fatigue. Clinical examination, MRI, and electromyography gave no other explanation to her progressive muscular weakness and fatigue than postpolio syndrome. She was treated with 400 mg/kg immunoglobulin intravenously for five consecutive days. RESULTS: At follow-up two and three months later, she had a considerable increase in isokinetic muscle strength in knee extension and flexion on the right side, and experienced less fatigue. INTERPRETATION: This case suggests that stabilisation of an autoimmune dysfunction may be a therapeutic option in postpolio syndrome.
BACKGROUND: Patients with polio often experience new symptoms (muscle weakness, pain, fatigue and respiratory problems) many years after the acute disease. This study examined possible interactions between lifestyle factors (overweight, physical inactivity, smoking) and late polio with new symptoms. METHODS: A total of 148 patients hospitalized for acute polio in 1950-1954 at Haukeland University Hospital, Norway and 128 patients, hospitalized for acute polio in 1958 at Tartu University Hospital, Estonia responded to a mailed questionnaire regarding lifestyle and late polio with new symptoms. Multiple regression analysis, two samples t-test and chi-square analysis were undertaken. RESULTS: Mean body mass index (BMI) and percentage of smokers did not differ in the two cohorts, while polio patients were physically less active in Estonia. The physically active patients in both cohorts had significantly lower odds for experiencing polio-related late muscle pain (OR = 0.21; 95% CI = 0.08-0.55) and fatigue (OR = 0.32; 95% CI = 0.14-0.75). With increasing age the patients had significantly higher odds for experiencing new muscle weakness (OR = 1.03; 95% CI = 1.00-1.07), fatigue (OR = 1.04;95% CI = 1.01-1.07) and breath shortness (OR = 1.04; 95% CI = 1.00-1.07). CONCLUSION: Physically inactive patients are at a higher risk for late polio-related symptoms. An active lifestyle should be recommended for patients with polio sequels.
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Poliovirus (PV) subjected to genetic characterization is often isolated from faecal carriage. Such virus is not necessarily identical to the virus causing paralytic disease since genetic modifications may occur during replication outside the nervous system. We have searched for poliovirus genomes in the 14 fatal cases occurring during the last epidemics in Norway in 1951-1952. A method was developed for isolation and analysis of poliovirus RNA from formalin-fixed and paraffin-embedded archival tissue. RNA was purified by incubation with Chelex-100 and heating followed by treatment with the proteinase K and chloroform extraction. Viral sequences were amplified by a reverse transcriptase-polymerase chain reaction (RT-PCR), the products subjected to TA cloning and sequenced. RNA from the beta-actin gene, as a control, was identified in 13 cases, while sequences specific for poliovirus were achieved in 11 cases. The sequences from the 2C region of poliovirus were rather conserved while those in the 5'-untranslated region were variable. The developed method should be suitable also for other genetic studies of old archival material.
Poliomyelitis is a viral infection that causes flaccid paralysis in approximately 1% of cases. The Fc receptors for immunoglobulin G (FcgammaR) are associated with modifying effects of several infectious and autoimmune diseases. To assess the influence of FcgammaR polymorphisms on the acute and late course of poliomyelitis, 110 Norwegian patients with well-defined histories of acute poliomyelitis were genotyped, of whom 50 suffered from the postpolio syndrome (PPS). In comparison with healthy control subjects without a history of poliomyelitis, significantly fewer patients had the FcgammaRIIIA genotype V/V (P<.01). However, this genotype was not an independent risk factor for PPS. The FcgammaRIIA and IIIB genotypes and allele frequencies did not differ between the patients and control subjects. The FcgammaRIIIA V/V genotype may lower the risk for contracting acute poliomyelitis through better clearance of poliovirus.
OBJECTIVE: To examine patients with previous nonparalytic poliomyelitis in search of muscle atrophy, weakness, and other late symptoms of poliomyelitis. DESIGN: A mailed questionnaire followed up with neurologic and neurophysiologic examinations of respondents who reported symptoms possibly related to the late sequelae of polio. SETTING: Neurology department at a university hospital. PARTICIPANTS: Thirty-nine of 47 patients diagnosed with nonparalytic poliomyelitis and hospitalized at a Norwegian hospital between 1950 and 1954, during the Norwegian polio epidemic. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Electromyography to determine function of the anterior tibialis, vastus lateralis, and biceps brachii muscles; nerve conduction studies of the sural, peroneal, and tibial nerves; motor and sensory nerve conduction velocity, and compound muscle and sensory nerve action potentials, and distal latencies. RESULTS: Twenty-five of 47 patients (53.2%) reported symptoms possibly related to the late sequelae of poliomyelitis. Eight of 20 examined symptomatic patients had normal neurologic and neurophysiologic findings, whereas 9 others had other medical conditions that could explain the symptoms. Three patients (6.7%) had neurologic and neurophysiologic findings and development of symptoms consistent with motoneuron damage. CONCLUSION: Some nonparalytic patients may have subclinical acute motoneuron damage with subsequent development and manifestation of motor weakness and neuromuscular symptoms many years later. These symptoms should be considered a differential diagnosis in patients who have a history of nonparalytic poliomyelitis.