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Biomedical subjects

J G McLeod

Publications and source records attributed to J G McLeod.

At least 19 recordsLinked to original sources
PubMed1995

Synergy between antibody and P2-reactive T cells in experimental allergic neuritis.

Studies were conducted in experimental allergic neuritis (EAN) to evaluate the possible interaction of cellular and humoral immune mechanisms in the demyelinating process. EAN was induced in Lewis rats by passive transfer of T cells reactive to P2 myelin protein or by active immunisation with whole myelin. Animals were then given systemic antimyelin antibody or control serum and assessed clinically, electrophysiologically and with semiquantitative histological studies. Animals given intraperitoneal (i.p.) P2-reactive T cells and systemic antimyelin antibody developed much more severe disease than those given i.p. T cells alone (P < 0.001). In actively immunised animals, the addition of systemic antimyelin antibody did not significantly alter disease severity. We believe the more severe disease in animals receiving T cells and antimyelin antibody reflects synergy between cellular and humoral immune mechanisms whereby neural antigen-specific T cells breach the blood-nerve barrier, allowing demyelinating antibody access to the endoneurium. In EAN induced by active immunisation with whole myelin it is likely that both B and T cell activation occurs and that the more severe demyelination characteristic of this disease reflects the involvement of both humoral and cellular immunity.

Animals↗
PubMed1995

Peripheral neuropathy associated with simvastatin.

Four patients are described who developed sensorimotor neuropathy while being treated with simvastatin and had complete or partial resolution of clinical abnormalities after withdrawal of treatment. In one case onset was within days of commencing treatment, but in two cases symptoms did not develop for two years. The electrophysiological and pathological features of the neuropathy were those of axonal degeneration. Clinical evidence of proximal and distal weakness and muscle fasciculations and persistent abnormalities of sensory conduction after recovery suggest the possibility of toxic damage to anterior horn cells and dorsal root ganglia. Thirty eight other cases with symptoms suggestive of peripheral neuropathy have been reported to the Australian Adverse Drug Reactions Advisory Committee, 22 of whom recovered after cessation of treatment; in five cases there was recurrence after re-exposure to the drug. Simvastatin should be considered among the causes of peripheral neuropathy, and the drug should be withdrawn if patients receiving it develop muscle weakness or sensory disturbances.

Adult↗
PubMed1994

A frame shift mutation in the PMP22 gene in hereditary neuropathy with liability to pressure palsies.

Hereditary neuropathy with liability to pressure palsies (HNPP) has been a associated with a deletion of 1.5 megabases of chromosome 17p. One of four biopsy proven HNPP families that we have studied did not possess this deletion. As the deleted DNA region includes the coding region for a peripheral myelin gene (PMP22), we used single strand conformation analysis to examine this gene for mutations in the non-deleted HNPP family. An abnormal fragment in exon 1 was identified, and sequencing revealed a two base pair deletion in all affected family members. The deletion results in a frame shift, providing strong evidence that this gene has an important role in the pathogenesis of the disease.

Base Sequence↗
PubMed1994

Peroneal muscular atrophy with pyramidal tract features (hereditary motor and sensory neuropathy type V): a clinical, neurophysiological, and pathological study of a large kindred.

A large family with autosomal dominant inheritance of peroneal muscular atrophy, associated with extensor plantar responses in some cases, has been studied. Onset was usually in the first two decades and spasticity was not a feature. Nerve conduction studies in 21 cases and light and electron microscope findings on six sural nerve biopsies were similar to those in hereditary motor and sensory neuropathy type II.

Adolescent↗
PubMed1992

Invited review: autonomic dysfunction in peripheral nerve disease.

The autonomic nervous system is affected in most peripheral neuropathies, but only in a small number of conditions, such as diabetes, amyloidosis, Guillain-Barré syndrome, porphyria, and familiar dysautonomia, is autonomic dysfunction of clinical importance. The pathological changes in the peripheral autonomic nervous system are similar to those in the peripheral somatic nerves. Autonomic disturbances are most likely to occur when there is acute demyelination or damage to small myelinated and unmyelinated fibers. Autonomic investigations should include tests of both sympathetic and parasympathetic function. Treatment consists of management of the underlying cause of peripheral neuropathy, physical and pharmacological measures.

Animals↗
PubMed1992

Autonomic dysfunction in peripheral nerve disorders.

The autonomic nervous system is affected by most conditions that cause peripheral neuropathy. Autonomic dysfunction may be clinically significant in some conditions such as diabetes, amyloidosis, Guillain-Barré syndrome and porphyria, but in many the autonomic disturbances are of only minor clinical importance. Clinical tests of both sympathetic and parasympathetic function are necessary to establish the diagnosis.

Autonomic Nervous System↗
PubMed1991

Autonomic function in hereditary motor and sensory neuropathy (Charcot-Marie-Tooth disease)

Autonomic tests of heart rate and blood pressure control using both invasive and noninvasive techniques were performed on 11 patients with hereditary motor and sensory neuropathy (HMSN) types 1, and 4 patients with HMSN type 2. The results were compared with those of 76 control subjects. No significant difference was found between the patient and control groups. Impairment of sweating on the extremities was found in patients with HMSN types 1 and 2, consistent with distal degeneration of sympathetic fibers in peripheral nerves, but there were no abnormalities of cardiovascular reflex control mechanisms.

Adolescent↗
PubMed1991

Vasculitic neuropathy. A clinical and pathological study.

The clinical, electrophysiological and pathological features and prognosis of 34 patients with peripheral neuropathy caused by necrotizing vasculitis were evaluated. The causes included polyarteritis nodosa and its Churg-Strauss variant, rheumatoid arthritis, undifferentiated connective tissue disease, Wegener's granulomatosis, primary Sjögren's disease, and chronic lymphocytic leukaemia with cryoglobulinaemia; 2 patients had no evidence of systemic vasculitis. Mononeuritis multiplex was the most common clinical manifestation, followed by asymmetrical polyneuropathy and distal symmetrical polyneuropathy. Pain was a frequent symptom. Nerve conduction studies were abnormal in all cases, and in 3 patients there was conduction block or severe slowing of motor conduction. Necrotizing vasculitis was present in sural nerve biopsies of most cases, and severe active axonal degeneration was a dominant feature. Immunofluorescent staining of blood vessels for immunoglobulin, C3 and fibrinogen was positive in all cases in which it was performed, even when there was no cellular infiltration. All patients were treated with prednisone alone or in combination with other immunosuppressive agents, or with plasmapheresis. Long-term follow-up studies demonstrated that although the peripheral neuropathy usually improved and caused only mild to moderate functional disability, the long-term prognosis of the systemic disease was poor with a 5-yr survival of only 37%.

Adult↗
PubMed1991

Autonomic function in Friedreich's ataxia.

Autonomic function studies were performed on 15 patients with Friedreich's ataxia, and the results compared with those of 76 healthy subjects. There was an increase in resting supine heart rate, attributed to cardiac abnormalities. Other tests of sympathetic and parasympathetic function were normal. The normal autonomic function studies are consistent with the pathological findings of degeneration predominantly of large diameter myelinated fibres with sparing of small myelinated and unmyelinated fibres.

Adolescent↗
PubMed1991

Superior sagittal sinus thrombosis.

Seven cases of superior sagittal sinus thrombosis seen at Royal Prince Alfred Hospital over the 10 year period 1979 to 1989 have been reviewed. Diagnosis was confirmed by angiography, CT scan or autopsy. The average age was 33 years (16 to 47 years). Five of the patients were female and 2 male. On CT scan the 'empty delta' sign, present in 4 cases, was the most specific diagnostic feature. The underlying causes included primary thrombocythaemia, homocystinuria, post-angiographic investigation of an arteriovenous malformation, and oral contraceptives. In 2 cases no cause was found. Headache was the commonest and earliest symptom, being followed in frequency by convulsions and hemiparesis. Hemiparesis was the commonest sign observed, followed by papilloedema, cranial nerve palsies and impaired level of consciousness. Five of the patients developed signs and symptoms of raised intracranial pressure prior to the appearance of focal neurological deficits, mostly likely due to propagation of the thrombosis to cortical veins. There have been no controlled trials of therapy; however it is important to treat raised intracranial pressure rapidly and effectively, and although the role of anticoagulants remains controversial, their early use may be indicated when there is no radiological evidence of haemorrhage.

Adolescent↗
PubMed1990

Anosmia after doxycycline use.

We report the case of a man who developed anosmia while taking doxycycline tablets for a skin disorder. Two other cases of parosmia occurring in association with doxycycline have been reported to the Adverse Drug Reactions Advisory Committee of the Commonwealth Department of Community Services and Health since 1972. Disturbances of taste but not olfaction have been reported with tetracycline use in the past.

Acne Vulgaris↗
PubMed1990

Magnetic resonance imaging in clinically-definite multiple sclerosis.

Forty-two patients with clinically-definite multiple sclerosis were examined by magnetic resonance imaging using a 1.5-T instrument. Magnetic resonance imaging detected an abnormality in 90% of patients. In four patients, no lesions were demonstrated. The number, size and site of the lesions by magnetic resonance imaging were compared with the patients' clinical status and other variables. The Kurtzke disability status scale score increased in patients with corpus callosum atrophy, and brainstem and basal ganglia lesions, and correlated with the total number of lesions. No correlation was shown between the findings of magnetic resonance imaging and disease duration, age, sex or pattern-reversal visual-evoked potentials. This article highlights the variety of magnetic resonance images that is obtained in patients with clinically-definite multiple sclerosis.

Adult↗
PubMed1990

Autonomic function and unmyelinated fibers in chronic inflammatory demyelinating polyradiculoneuropathy.

Because autonomic function may be abnormal in some demyelinating peripheral neuropathies, it has been studied with a number of noninvasive and invasive tests in 14 patients with chronic inflammatory demyelinating polyradiculoneuropathy. There were abnormalities of the 30:15 ratio in 3 patients and an abnormal thermoregulatory sweat test in 5 patients. These findings are indicative of mild parasympathetic and sympathetic dysfunction. Minor pathological changes in unmyelinated fibers were demonstrated on morphometric examination of sural nerves of 10 patients.

Adolescent↗
PubMed1990

Effect of neural activity on skeletal muscle phosphoproteins.

A number of phosphoproteins were found in the soluble fraction of rat skeletal muscle by two-dimensional polyacrylamide gel electrophoresis (PAGE). The pattern of some of these phosphoproteins differed in fast (extensor digitorum longus, EDL) or slow (soleus) muscles, was dependent on normal innervation, and was altered with denervation. In order to determine if the pattern was maintained by electrical activity or trophic factors, we compared the effect of electrical block by local neural application of tetrodotoxin with the effect of complete nerve section. Both methods produced similar alterations in phosphoproteins, indicating that the pattern is dependent on nerve activity, not trophic factors. Such phosphoproteins are possible mediators of neural activity on gene expression.

Animals↗