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Biomedical subjects

J J Halperin

Publications and source records attributed to J J Halperin.

At least 37 records · Page 2Linked to original sources
PubMed1989

Carpal tunnel syndrome in Lyme borreliosis.

Neurophysiologic evidence of median nerve entrapment in the carpal tunnel was present in 25% of patients with late Lyme borreliosis. Sixty-eight of 76 consecutive, prospectively studied patients with late Lyme underwent neurophysiologic testing. Nineteen reported intermittent hand paresthesias; 17 had neurophysiologically confirmed carpal tunnel syndrome. This was not consistently associated with clinically apparent wrist arthritis or with neurophysiologically evident peripheral neuropathy. We conclude that a significant proportion of patients with late Lyme borreliosis develop carpal tunnel syndrome.

Adult↗
PubMed1989

Lyme neuroborreliosis: central nervous system manifestations.

We evaluated 85 patients with serologic evidence of Borrelia burgdorferi infection. Manifestations included encephalopathy (41), neuropathy (27), meningitis (2), multiple sclerosis (MS) (6), and psychiatric disorders (3). We performed lumbar punctures in 53, brain MRI in 33, and evoked potentials (EPs) in 33. Only patients with an MS-like illness had abnormal EPs, elevated IgG index, and oligoclonal bands in the cerebrospinal fluid. Twelve of 18 patients with encephalopathy, meningitis, or focal CNS disease had evidence of intrathecal synthesis of anti-B burgdorferi antibody, compared with no patients with either MS-like or psychiatric illnesses, and only 2/24 patients with neuropathy. MRIs were abnormal in 7/17 patients with encephalopathy, 5/6 patients with an MS-like illness, and no others. We conclude that (1) intrathecal concentration of specific antibody is a useful marker of CNS B burgdorferi infection; (2) Lyme disease causes an encephalopathy, probably due to infection of the CNS; (3) MS patients with serum immunoreactivity against B burgdorferi lack evidence of CNS infection with this organism.

Acute Disease↗
PubMed1989

Nervous system manifestations of Lyme disease.

Neurologic involvement is commonplace in Lyme borreliosis. Neuropathies can be acute or chronic, focal or disseminated, but are predominantly axonal. CNS infection can also be acute or indolent, focal or disseminated; meningitis, encephalitis, and cranial nerve palsies occur. A mild encephalopathy is also common, but only occasionally due to CNS infection.

Central Nervous System Diseases↗
PubMed1988

Seronegative Lyme disease. Dissociation of specific T- and B-lymphocyte responses to Borrelia burgdorferi.

The diagnosis of Lyme disease often depends on the measurement of serum antibodies to Borrelia burgdorferi, the spirochete that causes this disorder. Although prompt treatment with antibiotics may abrogate the antibody response to the infection, symptoms persist in some patients. We studied 17 patients who had presented with acute Lyme disease and received prompt treatment with oral antibiotics, but in whom chronic Lyme disease subsequently developed. Although these patients had clinically active disease, none had diagnostic levels of antibodies to B. burgdorferi on either a standard enzyme-linked immunosorbent assay or immunofluorescence assay. On Western blot analysis, the level of immunoglobulin reactivity against B. burgdorferi in serum from these patients was no greater than that in serum from normal controls. The patients had a vigorous T-cell proliferative response to whole B. burgdorferi, with a mean ( +/- SEM) stimulation index of 17.8 +/- 3.3, similar to that (15.8 +/- 3.2) in 18 patients with chronic Lyme disease who had detectable antibodies. The T-cell response of both groups was greater than that of a control group of healthy subjects (3.1 +/- 0.5; P less than 0.001). We conclude that the presence of chronic Lyme disease cannot be excluded by the absence of antibodies against B. burgdorferi and that a specific T-cell blastogenic response to B. burgdorferi is evidence of infection in seronegative patients with clinical indications of chronic Lyme disease.

Adolescent↗
PubMed1988

Treatment of late Lyme borreliosis--randomised comparison of ceftriaxone and penicillin.

23 patients with clinically active late Lyme disease were randomly assigned to intravenous treatment with either penicillin or ceftriaxone. Of the 10 treated with penicillin, 5 were judged treatment failures; of the 13 who received ceftriaxone, only 1 did not respond. An additional 31 patients were subsequently treated with ceftriaxone 4 g/day (n = 17) or 2 g/day (n = 14); success rates in both groups were comparable to those in the cohort randomised to ceftriaxone. Patients unresponsive to ceftriaxone were more likely to have received corticosteroid treatment.

Administration, Oral↗
PubMed1988

New chemotherapeutic approaches in the treatment of Lyme borreliosis.

1. It was demonstrated that while B. burgdorferi may be sensitive to relatively small concentrations of penicillin and ceftriaxone, the organism is killed slowly. This implies that, as in syphilis, prolonged blood levels of these drugs may be necessary in order to ensure cure. In contrast, the activity of tetracycline is more rapid in its action but is more dependent on drug concentration achieved. Unfortunately, the MIC and MBC for some strains are at or above the peak level achieved under optimal conditions. 2. Increasing the concentrations of penicillin or ceftriaxone above the MIC for the organism has little effect on the rate of killing. In contrast, the killing by tetracycline can be augmented by increasing concentrations of the drug. 3. Ceftriaxone is more active than penicillin, as measured by MIC, against the five strains of B. burgdorferi tested. 4. Ceftriaxone was efficacious in the treatment of Lyme borreliosis, which was recalcitrant to penicillin therapy. In a randomized trial comparing ceftriaxone to high-dose penicillin therapy, ceftriaxone was significantly more efficacious than penicillin in the treatment of the late complications of Lyme borreliosis.

Anti-Bacterial Agents↗
PubMed1987

Failure of tetracycline therapy in early Lyme disease.

We describe the clinical courses of 5 patients with Lyme disease who developed significant late complications, despite receiving tetracycline early in the course of their illness. All 5 patients had been treated for erythema chronicum migrans with a course of tetracycline that met or exceeded current recommendations. The late manifestations of Lyme disease included arthritis, cranial nerve palsy, peripheral neuropathy, chronic fatigue, and changes in mental function. Our findings suggest that the use of tetracycline at a dosage of 250 mg, 4 times a day for 10 days, as a treatment for early Lyme disease should be reconsidered. To determine optimal therapy for early Lyme disease, a study that compares an increased dosage of tetracycline with alternative treatments is indicated.

Adolescent↗
PubMed1987

Lyme disease: cause of a treatable peripheral neuropathy.

Peripheral nerve dysfunction was demonstrated in 36% of patients with late Lyme disease. Of 36 patients evaluated, 14 had prominent limb paresthesias. Thirteen of these had neurophysiologic evidence of peripheral neuropathy; neurologic examinations were normal in most. Repeat testing following treatment documented rapid improvement in 11 of 12. We conclude that this neuropathy, which is quite different from the infrequent peripheral nerve syndromes previously described in this illness, is commonly present in late Lyme disease. This neuropathy presents with intermittent paresthesias without significant deficits on clinical examination and is reversible with appropriate antibiotic treatment. Neurophysiologic testing provides a useful diagnostic tool and an important measure of response to treatment.

Adult↗
PubMed1987

Lyme meningoencephalitis: report of a severe, penicillin-resistant case.

Although Lyme disease frequently attacks the central nervous system, this involvement is rarely severe, and high-dose intravenous penicillin usually is adequate treatment. The patient we describe developed severe Lyme meningoencephalitis despite receiving a full course of penicillin, and his condition continued to deteriorate after reinstitution of this treatment. Intravenous chloramphenicol was used successfully and resulted in a substantial improvement.

Adult↗
PubMed1984

Communicating hydrocephalus and lysosomal inclusions in mannosidosis.

A 32-year-old man with mannosidosis had a gait disorder develop that was associated with communicating hydrocephalus. The gait disorder improved with ventriculoperitoneal shunting, but proximal muscle weakness remained. Biopsy specimens of muscle and nerve disclosed typical lysosomal inclusions in both tissues, as well as selective loss of unmyelinated axons.

Adult↗
PubMed1984

Sympathetic skin response--a method of assessing unmyelinated axon dysfunction in peripheral neuropathies.

The sympathetic skin response (SSR) was measured in 33 patients with peripheral neuropathies and in 30 normal control subjects. Abnormalities of the response were correlated with clinical, pathologic, and EMG observations. The response was usually absent in axonal neuropathies, but present in demyelinating disorders. Abnormalities of the sympathetic skin response did not correlate well with clinical evidence of dysautonomia, but were a reliable indicator of disorders affecting unmyelinated axons.

Adolescent↗
PubMed1983

Development of synaptic junctions in cerebellar glomeruli.

In the glomerular synapses of developing mouse cerebellar cortex, 2 components of the synaptic junctions assemble independently in the immature granule cell dendrites, and then combine. 'Initial' junctions between mossy fiber axons and immature granule cell dendrites have presynaptic and postsynaptic electron-dense fuzz and a widened synaptic cleft, but lack the aggregate of intramembrane particles associated with the extracellular half of the postsynaptic membrane which characterizes mature synaptic junctions. In the vicinity of 'initial junctions' there are particle aggregates which resemble those at mature synaptic junctions, but which are less densely packed and which are not associated with the other features of a junction. The constituent particles of these aggregates move to the sites of 'initial junctions' to combine with them and form 'immature synaptic junctions'. Many of these immature junctions are larger in area than mature synaptic junctions. The immature junctions accumulate a fairly uniform complement of intramembrane particles, which increase in packing density as the junctions decrease in area and attain smaller, adult size.

Animals↗