Biomedical subjects

A R Pachner

Publications and source records attributed to A R Pachner.

64 records · Page 4Linked to original sources

PubMed1985

Facial paralysis in Lyme disease.

Lyme disease is a multisystemic illness caused by a tick-borne spirochete. Once considered unique to the Connecticut coastline, thousands of cases are now documented throughout the United States, northern Europe, and Australia. Unilateral and bilateral facial paralysis may occur in up to 11% of patients with Lyme disease. This paper reviews the clinical course, distinguishing features, and outcome of 124 such palsies in 101 patients seen between 1975 and 1984. The 99.2% spontaneous recovery rate demonstrates the unequivocally excellent prognosis of this palsy and confirms that operative intervention is not indicated. The otolaryngologist should consider this etiology in all otherwise idiopathic facial paralyses, especially when presenting in summer months in endemic areas, or when bilateral. Positive Lyme disease spirochete titers are helpful in the diagnosis. We believe antibiotics should be given to patients with this facial palsy in order to treat any other concurrent manifestations of the illness and to prevent subsequent complications.

Adolescent↗

PubMed1984

In vitro and in vivo actions of acetylcholine receptor educated suppressor T cell lines in murine experimental autoimmune myasthenia gravis.

Immunization of C57Bl/6 mice with Torpedo acetylcholine receptor (AChR) leads to EAMG, experimental autoimmune myasthenia gravis, with characteristic clinical, electrophysiological, and immune features. Present in the lymphoid organs of mice with EAMG are AChR specific suppressor T cells: these cells can be grown in vitro as T cell lines. These lines are able to suppress the in vitro response to AChR, and can suppress the in vivo development of EAMG.

Animals↗

PubMed1983

Neurologic abnormalities of Lyme disease: successful treatment with high-dose intravenous penicillin.

Twelve patients were treated with high-dose intravenous penicillin for neurologic abnormalities of Lyme disease. Headache, stiff neck, and radicular pain usually began to subside by the second day of therapy and were often gone by 7 to 10 days. Five of the 12 patients continued to have intermittent mild headache for several more weeks, but no patient relapsed after therapy was stopped. Compared to 15 previous patients treated with prednisone alone, the duration of meningitic syndrome was significantly shorter in those given penicillin (mean duration, 1 versus 29 weeks, p less than 0.000001). However, in both groups, a mean of 7 to 8 weeks was required for complete recovery of motor deficits. Despite antibiotic therapy, 3 of the 12 patients treated with penicillin continued to have frequent arthralgias, musculoskeletal pain, and fatigue. We conclude that high-dose intravenous penicillin is effective therapy for neurologic abnormalities of Lyme disease.

Adolescent↗

PubMed1983

The relation of clinical disease to antibody titre, proliferative response and neurophysiology in murine experimental autoimmune myasthenia gravis.

Murine myasthenia is a relatively faithful model of the human disease. We studied anti-AChR antibody titres, lymphocyte proliferative response to AChR, characteristic electromyographic (EMG) abnormalities and muscle strength at weekly intervals after immunization of C57B16J mice with Torpedo AChR. The boosting immunization at 1 month after the primary immunization resulted in a progressive increase of anti-AChR IgG antibodies, but caused a marked drop in the proliferative response. Although characteristic EMG abnormalities occurred in nearly all immunized mice, clinical disease appeared very late or not at all. These data parallel findings in human myasthenia.

Acetylcholine↗

PubMed1982

Nerve stimulation test in murine experimental autoimmune myasthenia gravis.

Use of the mouse model of myasthenia gravis (murine EAMG), ideally suited for immunological study, has been hampered by the relatively mild character of the disease and by the extended time and effort required for inducing severe disease. Electromyographic measurement of the compound action potential after repetitive stimuli, the nerve stimulation test, was evaluated for its ability to diagnose neuromuscular transmission defects in mice immunized with Torpedo acetylcholine receptor. With the combination of provocative maneuvers and raising of the body temperature, EAMG could be diagnosed in nearly all immunized animals a few weeks after immunization, whereas clinical evaluation of muscle weakness was positive in less than half of immunized mice months after the first immunization. Thus, EMG provides a means of objective evaluation of the disease and attempts at its experimental modification.

Animals↗

PubMed1976

Cytokine inhibition of DNA synthesis: effect on cyclic adenosine monophosphate in lymphocytes.

A greater than twofold increase in intracellular adenosine 3',5'-monophosphate (cyclic AMP) inhibited DNA synthesis, in stimulated rat lymphocytes. A two- to fourfold rise of intracellular cyclic AMP, starting at 16 hours, was produced by purified inhibitor od DNA synthesis added to such cells either at 0 or 16 hours, in close association with the initiation of DNA synthesis.

Animals↗

PubMedDate not supplied

Murine Lyme borreliosis: route of inoculation determines immune response and infectivity.

Outer surface protein A OspA is the major outer surface protein of B. burgdorferi, the causative agent of Lyme disease, and has been advocated as a vaccine candidate. It is recognized late or not at all in the course of human Lyme disease, but has been identified as a major antigenic epitope for the anti-spirochetal immune response in a number of experimental models of B. burgdorferi infection. We injected B.burgdorferi into mice and tested the appearance of immunoreactivity to OspA by Western blotting. Three routes of infection were studied; other variables investigated were inoculum size and isolate of spirochete and strain of mouse. OspA immunoreactivity, as determined by Western blotting, was readily elicited by injection of sonicates under almost any condition. Intraperitoneal or intravenous injection of infectious spirochetes, especially at infective inoculum sizes, or injection of the noninfectious B31 isolate by any route, resulted in OspA immunoreactivity. However, mice from the three strains tested infected intradermally did not develop significant OspA immunoreactivity, but instead developed strong responses to B.burgdorferi proteins of different molecular weights. These data suggest that during infection within the skin after intradermal inoculation, the OspA protein may be altered in some way to make it less immunogenic than when it is presented to the immune system under other circumstances.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Neurologic manifestations of Lyme disease, the new "great imitator".

The causative agent of Lyme disease, Borrelia burgdorferi, is a highly neurotropic organism that not only can produce symptomatic neurologic disease but also can exist dormant within the central nervous system (CNS) for long periods. Two distinct types of neuroborreliosis occur at different stages of Lyme disease. Second-stage Lyme meningitis resembles aseptic meningitis and is often associated with facial palsies, peripheral nerve involvement, and/or radiculopathies. Lyme meningitis may be the first evidence of Lyme disease, occurring without a history of erythema chronicum migrans or flu-like illness. Third-stage parenchymal involvement causes a multitude of nonspecific CNS manifestations that can be confused with conditions such as multiple sclerosis, brain tumor, and psychiatric derangements. Manifestations of CNS parenchymal involvement in Lyme disease are generally associated, however, with a history of erythema chronicum migrans, meningitis, or carditis. Both second- and third-stage Lyme neuroborrelioses are commonly misdiagnosed because they are relatively uncommon and because they mimic many better-known disorders.

Brain Diseases↗

PubMedDate not supplied

Experimental models of myasthenia gravis: lessons in autoimmunity and progress toward better forms of treatment.

The nicotinic acetylcholine receptor (AChR) is a large membrane protein found in muscle cells. It is involved in the transformation of acetylcholine packets into a membrane depolarization, which thereby leads to a muscle twitch. This large, complex molecule is the target of the autoimmune attack in myasthenia gravis, and much has been learned in the past decade about myasthenia by the induction of autoimmunity to AChR in experimental animals. Experimental autoimmune myasthenia gravis (EAMG) has been produced in a variety of animals by immunization with AChR or AChR-like material, or by the passive transfer of anti-AChR antibodies or lymphocytes from afflicted animals into normal animals. EAMG is a remarkably faithful model of human myasthenia and has provided much information about how the immune response to AChR progresses and how weakness and damage to the neuromuscular junction ensure. EAMG has also allowed the development of a number of revolutionary forms of treatment in which only the abnormal response to AChR is restrained, and other necessary immune functions are left intact. These advances in treatment are not far from being tested in human myasthenia gravis. The experience gained in applying these concepts in EAMG and human myasthenia will be helpful in developing similar forms of treatment for other autoimmune diseases.

Animals↗

PubMedDate not supplied

Neurological findings of Lyme disease.

Neurologic involvement of Lyme disease typically consists of meningitis, cranial neuropathy, and radiculoneuritis, alone or in combination, lasting for months. From 1976 to 1983, we studied 38 patients with Lyme meningitis. Headache and mild neck stiffness, which fluctuated in intensity, and lymphocytic pleocytosis were the common findings. Half of the patients also had facial palsies, which were unilateral in 12 and bilateral in seven. In addition, 12 patients had motor and/or sensory radiculoneuropathies; asymmetric weakness of extremities was the most common finding. Although incomplete presentations of neurologic involvement of Lyme disease may be confused with other entities, the typical constellation of neurologic symptoms represents a unique clinical picture.

Adolescent↗