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Biomedical subjects

A J Sumner

Publications and source records attributed to A J Sumner.

At least 55 records · Page 3Linked to original sources
PubMed1987

Bipolar recording of short-latency somatosensory evoked potentials after median nerve stimulation.

Generators of median short-latency somatosensory evoked potentials were studied with three orthodiagonal pairs of bipolar electrodes. N11 was attributed to the dorsal root and dorsal column volleys. N13 had at least two subcomponents, generator dipoles of which are directed horizontally (N13a) and axially (N13b). N13a was generated in the lower cervical cord. N13b (bipolar) and P14 far-field (noncephalic reference) appeared to originate in the cuneate nucleus or spinocerebellar tracts as well as in the medial lemniscus. Bipolar recordings were useful in localizing cervical cord lesions, which was impossible in conventional monopolar recordings.

Adult↗
PubMed1984

The role of myelin P2 protein in the production of experimental allergic neuritis.

Myelin P2 protein has been proposed as the primary antigen in whole myelin-induced experimental allergic neuritis (EAN). We investigated the neuritogenic properties of P2 by sensitizing Lewis rats with complete Freund's adjuvant (CFA) containing P2, P2 plus phosphatidyl serine, or whole myelin containing an equivalent amount of P2. Animals were examined using a battery of clinical, electrophysiological, immunological, and morphological methods. Myelin-immunized rats developed the characteristic features of EAN. P2-sensitized rats developed a similar but much less intense disorder. When rats were sensitized with P2 in the presence of phosphatidyl serine, however, they developed radiculoneuropathy that was indistinguishable from myelin-induced EAN. Inoculation with phosphatidyl serine plus complete Freund's adjuvant or complete Freund's adjuvant alone had no detectable effect on peripheral nerves. These studies demonstrate that sensitization of rats with a single myelin antigen, P2 protein, is sufficient to induce the clinical, electrophysiological, and neuropathological features of EAN.

Animals↗
PubMed1984

Serum-mediated Schwann cell cytotoxicity in the Guillain-Barré syndrome.

To study the anti-Schwann cell activity of serum from patients with Guillain-Barré syndrome (GBS), we used a 51Cr-release cytotoxicity assay. Specific release of 51Cr mediated by GBS serum did not differ from that with normals or disease controls. Heating sera from GBS patients or controls at 56 or 50 degrees C for 30 minutes markedly decreased 51Cr specific release, which could not be restored by addition of either 10% guinea pig serum or normal human serum. Thus, both GBS and control serum contain heat-labile serum factors that can induce cytotoxic reactions by Schwann cells.

Blood↗
PubMed1982

Neurophysiological and neuropsychological function in mercury-exposed dentists.

In a study of the relation between cumulative exposure to mercury and chronic health impairment 298 dentists had their mercury levels measured by an X-ray fluorescence technique. Electrodiagnostic and neuropsychological findings in the dentists with more than 20 micrograms/g tissue mercury levels were compared with those of a control group consisting of dentists with no detectable mercury levels. 30% of the 23 high mercury dentists had polyneuropathies. No polyneuropathies were detected in the control group. The high mercury group had mild visuographic dysfunction; they also had more symptom-distress than did the control group. These findings suggest that the use of mercury as a restorative material is a health risk for dentists.

Adult↗
PubMed1982

Acute conduction block associated with experimental antiserum-mediated demyelination of peripheral nerve.

Intraneural injection of antisera from rabbits with high antigalactocerebroside antibody levels into rat sciatic nerve produced acute nerve conduction block. This was first apparent in some motor axons between 30 and 60 minutes after injection and progressed to completion within 2 to 4 hours. Concurrent morphological evidence of demyelination was present, but structural changes at the time of onset of block were mild and were restricted to the myelin and Schwann cell, particularly at the paranodal areas and Schmidt-Lanterman clefts. It is suggested that paranodal lesions could account for the observed conduction block.

Animals↗
PubMed1982

Conduction block in rat myelinated fibres following acute exposure to anti-galactocerebroside serum.

1. We have observed conduction in single rat spinal ventral root nerve fibres following acute topical application of anti-galactocerebroside serum.2. Conduction of nerve impulses was initially slowed and subsequently blocked at the site of serum exposure.3. Conduction block occurred within as little as 1 hr in more slowly conducting (20-30 m/sec) myelinated fibres but occurred later in fibres conducting more rapidly.4. Conduction block was preceded by a rise in internodal conduction time from the normal 20 musec to about 200 musec.5. At nodes exposed to serum, conduction block was invariably associated with greatly decreased depolarization; this was contrasted with nodes exposed to local anaesthetic or tetrodotoxin where conduction block occurred despite nodal depolarization well beyond threshold potential.6. Nodal capacitance and resistance were estimated from simultaneous recordings of membrane current and extracellular potential at blocked nodes exposed to local anaesthetic or tetrodotoxin (normal nodes) and at blocked nodes exposed to anti-galactocerebroside serum.7. For normal fibres of internodal length 0.8-1.1 mm, an upper limit estimate for average nodal capacitance was 2.6 +/- 0.3 pF and a lower limit estimate for average nodal resistance was 55 +/- 10 MOmega. There was an order of magnitude increase in the capacitance of nodes at which conduction block occurred following exposure to anti-galactocerebroside serum.8. We conclude that the early conduction block caused by anti-galactocerebroside serum is due to paranodal demyelination and that acute paranodal demyelination is sufficient to cause conduction block.

Animals↗
PubMed1982

The electrodiagnostic distinctions between chronic familial and acquired demyelinative neuropathies.

We compared the electrodiagnostic studies of 40 patients with chronic acquired demyelinative neuropathy and 18 patients with familial demyelinative neuropathy. Patients with acquired neuropathy had differential slowing of conduction velocity when distal latencies were compared with more proximal conduction velocities in the same nerve, when equivalent segments of different nerves were compared, and when dispersion of compound motor action potentials was examined. Conduction block was noted in some patients. Patients with familial disease had uniform conduction slowly of all nerve segments, and conduction block was not seen. Chronic acquired demyelinative neuropathy is characterized by multifocal slowing of nerve conduction, whereas familial demyelinative neuropathy is characterized by uniform conduction slowing.

Demyelinating Diseases↗
PubMed1982

Multifocal demyelinating neuropathy with persistent conduction block.

We describe five patients with a chronic asymmetric sensorimotor neuropathy most pronounced in the upper extremities with focal involvement of individual nerves. Diagnosis was established by electrophysiologic evidence of persistent multifocal conduction block. Sural nerve biopsy in three patients showed primarily demyelinating-remyelinating changes with varying degrees of fiber loss. Two patients had acute optic neuritis, indicating that the disorder was not always restricted to the peripheral nervous system. Two patients treated with corticosteroids improved, whereas three untreated patients had static deficits or steady progression of symptoms. Chronic multifocal demyelinating neuropathy with persistent conduction block seems to be a variant of chronic acquired demyelinating polyneuropathy and may be immunologically mediated.

Adult↗
PubMed1981

The physiological basis for symptoms in Guillain-Barré syndrome.

An experimental humorally induced focal demyelinative lesion of peripheral nerve is described. Associated with this lesion, conduction block appears rapidly--as early as 30 minutes in some axons--and progresses to completion within four hours. Small-diameter myelinated axons block before those of larger diameter. Recovery of conduction occurs in 6 to 15 days. This model provides a basis for understanding the time course of onset and recovery in acute Guillain-Barré syndrome and raises the possibility that a humoral mechanism might be important in the pathogenesis of the disease.

Animals↗
PubMed1980

Antiserum-mediated demyelination: relationship between remyelination and functional recovery.

A focal demyelinative lesion of peripheral nerve was produced by intraneural injection of either antiserum from rabbits with experimental allergic neuritis or experimental allergic encephalomyelitis or antiserum to galactocerebroside. We studied the relationship between clinical and electrophysiological recovery from this lesion and the morphological pattern of remyelination. Foot muscles on the the injected side weakened within an hour of injection and remained paralyzed for 7 days; strength gradually returned to normal by 16 days after injection. Electrophysiological conduction block, apparent within a few hours of injection, persisted for about 7 days. At 8 days we detected dispersed, very low amplitude muscle action potentials with long latency. Morphologically, demyelinated axons were surrounded by Schwann cells at 7 days after injection, but compacted myelin was not present. After 8 days, remyelinating axons became surrounded by thickening compacted myelin. The time of onset of remyelination and the rate of remyelination up to 14 days following the injection were independent of axon size. The onset of clinical and electrophysiological recovery from the lesion corresponded to the appearance of 2 to 8 myelin lamellae around each remyelinating axon. At 37 days after injection, when conduction velocities had returned to preinjection values, myelin thickness of remyelinating fibers had increased to approximately one-third that of control nerves.

Animals↗
PubMed1980

Distal neuropathy in experimental diabetes mellitus.

Although nerve conduction slowing is a well-accepted abnormality in rats with acute experimental diabetes, reports of neuropathological changes in diabetic rat nerves have been inconsistent. To examine this further, we studied electrophysiological and morphological features of posterior tibial nerves and their distal branches from four-week streptozotocin-induced diabetic rats and matched controls. Diabetic rat posterior tibial motor conduction was slowed (mean +/- 1 SD, 34.8 +/- 3.1 m/sec; controls, 41.2 +/- 2.5 m/sec), and evoked muscle response amplitudes were only half of control values. Using quantitative techniques, we documented a diminution in number of the largest myelinated fibers in otherwise normal mid posterior tibial nerves, with an increase in the smaller sizes, indicating either a degree of axonal atrophy or impaired fiber growth during development. The principal pathological finding was active breakdown of myelinated fibers in the most distal motor twigs of hindfoot muscles supplied by posterior tibial branches, with preservation of fibers in more proximal segments of these nerves. This anatomical lesion in diabetic nerves could account for both oberved conduction slowing and lowered muscle response amplitudes. A consistent feature in both diabetic and control mid lateral plantar nerves was a zone of demyelination that apparently occurs at this natural site of nerve entrapment in rats. Taken together, the pathological abnormalities of peripheral nerve in acute experimental diabetes are best explained as resulting from a distal axonopathy.

Animals↗
PubMed1979

Experimental allergic neuritis induced by sensitization with galactocerebroside.

Thirteen of 31 rabbits immunized repeatedly with bovine brain galactocerebroside developed experimental allergic neuritis, manifested by flaccid paresis and hypesthesia of four limbs, 2 to 11 months after the initial inoculation. Electrophysiological studies revealed multifocal conduction block of peripheral nerves. Perivenular demyelinative lesions associated with phagocytic mononuclear cells occurred in spinal ganglia, roots, and less frequently in distal nerves.

Animals↗
PubMed1976

Hereditary sensory neuropathy and tonic pupils.

The clinical features of two siblings with both hereditary sensory neuropathy and bilateral tonic pupils are described. Other neurologic disorders associated with tonic pupils are reviewed. Our patients appear to represent a unique instance of the association of disorders that primarily affect the ciliary and dorsal root ganglia.

Adult↗
PubMed1975

Glue-sniffing neuropathy.

Although industrial exposure to n-hexane is known to cause neuropathy, it is less well recognized that inhalation of n-hexane present in the vapors of some commercial contact cements is also neurotoxic to peripheral nerves. A young man with a long history of addictive glue-sniffing developed severe distal symmetrical polyneuropathy several months after switching to a cement containing n-hexane and gradually improved several months after switching to another cement containing no n-hexane. Fascicular biopsy of radial cutaneous nerve showed striking segmental distention of axons by neurofilamentous masses with secondary thinning of myelin sheath, paranodal myelin retraction, and widening velocities were correspondingly slow. We conclude that n-hexane used as a solvent in some contact cements may be neurotoxic when inhaled to excess and, further, that the neuropathy has characteristic electrophysiological and pathological features.

Acetates↗
PubMed1975

Physiological studies of the dying-back phenomenon. Muscle stretch afferents in acrylamide neuropathy.

(1) The responses of 1,001 medial gastrocnemius afferents with conduction velocities of 24-126 m/sec have been studied in cats with experimental acrylamide neuropathy. (2) Many units which conducted at velocities indicating that they innervated muscle stretch receptors failed to discharge during muscle stretch or contraction. In animals with mild neuropathy 10 per cent of 366 units were non-responsive. In animals with moderate or severe neuropathy the proportion of non-responsive units was 68 per cent of 315 fibres and 89 per cent of 320 fibres respectively. Group I fibres were involved to a greater extent than Group II fibres. (3) The distributions of identified functioning units with respect to conduction velocity were normal, indicating that acrylamide did not produce conduction slowing before failure of function. (4) Electrophysiological and histological findings indicate that acrylamide initially produces failure of impluse conduction and subsequent fibre breakdown in the terminal axon while normal impulse conduction is preserved more proximally.

Acrylamides↗
PubMed1975

Preservation of early discharge of muscle afferents in acrylamide neuropathy.

1. Responses to stretch and the 'early discharge' have been studied in acrylamide neuropathy in the expectation that functional block of the nerve terminals would allow these two processes to be dissociated. 2. Of 538 single group I and group II muscle afferents which were nonresponsive to stretch, ninety-nine displayed 'early discharge' which appeared to be identical with that described in normally functioning muscle stretch afferents. 3. Preservation of 'early discharge' in non-responsive fibres indicates these impulses do not arise from excitation of the muscle spindle itself. The evidence indicates that 'early discharge' is usually ephaptically excited by the muscle action potential.

Acrylamides↗
PubMed1975

Neuromuscular complications of acromegaly.

Seventeen consecutive acromegalic patients were evaluated for evidence of neuromuscular dysfunction and followed for 1 year after hypophysectomy. Before treatment, four patients had both a myopathy and the carpal tunnel syndrome, five had myopathy alone, four had carpal tunnel syndrome alone, and four had neither. The myopathy was caracterized by mild, strictly promixal weakness and flabbiness of muscles; electromyography revealed typical myopathic abnormalities, but serum enzymes and muscle biopsy usually were normal. The presence of myopathy or the carpal tunnel syndrrome could not be correlated with the magnitude of growth hormone elevation or any secondary endocrine derangement, but myopathy was associated with a longer duration of acromegaly. Carpal tunnel symptoms usually improved in the first 6 weeks after hypophysectomy, while myopathy improved more slowly and sometimes was detectable 1 year later.

Acromegaly↗