Is sarcocystosis common in Sydney?
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Female↗
Biomedical subjects
R Pamphlett
Publications and source records attributed to R Pamphlett.
Lead uptake in motor axons.
In an attempt to determine whether lead (Pb) in striated muscle can be taken up by motor axon, mice were injected intramuscularly with a 5% Pb nitrate solution, and the passage of Pb through the tissues was traced with electron microscopy. Thirty minutes after injection in the tibialis anterior muscle, Pb was seen at the sarcolemma and axolemma of the neuromuscular junction (NMJ) and in the adjacent sarcoplasmic reticulum (SR). Pb was also present in the axoplasm and mitochondria of terminal and preterminal motor axons. The presence of Pb was confirmed with x-ray elemental microanalysis. The results indicate that there is a pathway for intramuscular Pb to enter terminal motor axons. This supports the hypothesis that some forms of motor neuron disease (MND) may be due to axonal uptake and retrograde transport of Pb.
Animals↗
Brain stem serotonin-synthesizing neurons in Alzheimer's disease: a clinicopathological correlation.
The location and number of brain stem serotonin-synthesizing neurons were analyzed in 11 patients with Alzheimer's disease (AD) and 5 age-matched controls using immunohistochemical techniques. In addition, the number of neuritic plaques and neurofibrillary tangles in the cortex and brain stem raphe was evaluated, as was the number of Nissl-stained raphe neurons. AD patients could be classified into two groups based on their raphe pathology; patients with such pathology (AD+) and those without (AD-). The number of large raphe neurons correlated significantly with the number of serotonin-synthesizing neurons in control material, indicating that all large neurons were serotonergic. This relationship was not apparent in AD+ patients, in whom the number of serotonin-synthesizing neurons correlated with the number of neurofibrillary tangles in the raphe of these patients. This indicates that in AD+ patients the serotonin-synthesizing neurons were selectively affected. There was no correlation between raphe and cortical pathology or raphe pathology and patient sex, age, mini-mental score or depression score, even when such scores were weighted for the interval between testing and death. There was a trend for the raphe pathology to correlate with the age of onset and duration of dementia and the Blessed dementia score in AD+ patients. Most AD+ patients with severe raphe lesions had clinical dementia only, while AD- patients had additional clinical features. The raphe lesions were more dramatic in AD+ patients with a rapid progression of symptoms.
Aged↗
The effect of nerve crush and botulinum toxin on lead uptake in motor axons.
After lead (Pb) is injected into striated muscle it binds to the sarcolemma of the neuromuscular junction (NMJ) and crosses into the terminal axons of motor neurons. To find out whether this intra-axonal accumulation of Pb is due to active transport or to diffusion down a concentration gradient, Pb uptake into motor axons of mice was studied at active and inactive NMJs. Twenty-four hours after sciatic nerve crush, 0.1 ml of 5% lead nitrate was injected into the tibialis anterior muscle and 30 min later the location of Pb was sought with electron microscopy and X-ray elemental analysis. A greatly reduced amount of Pb entered the axons after nerve crush compared to non-nerve crush animals, indicating that an active NMJ is required for intra-axonal Pb accumulation. To test if Pb could be entering the axon via recycling vesicles, botulinum toxin (BoTx) was injected into the muscle 24 h before Pb injection. There was no difference in intra-axonal Pb uptake in control and BoTx-injected animals, indicating that Pb is unlikely to use recycled vesicles to enter the axon.
Animals↗
Antibodies against Sarcocystis and Toxoplasma in humans with the chronic fatigue syndrome.
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Animals↗
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↗
Sarcocystis infection of human muscle.
A 31-year-old man with fatigue and muscle aches was found to have protozoan cysts within the most painful muscle upon microscopic examination of biopsy material. Electron microscopic studies revealed the ultrastructural characteristics of the cysts to conform to those of the genus Sarcocystis. This report represents the first ultrastructural study of human tissue infection with Sarcocystis, which may be a rare cause of muscle aching in humans.
Adult↗
Infective endocarditis with inflammatory lesions in the peripheral nervous system.
A 64-year-old woman developed septicemia and a generalized peripheral neuropathy while being ventilated postoperatively. No cause for the neuropathy could be found during life. At autopsy she was found to have infective endocarditis and multifocal inflammatory lesions in the central and peripheral nervous systems, consistent with damage due to septic emboli. Infective endocarditis may be a cause of a generalized polyradiculoneuropathy and could be responsible for a proportion of cases of "critical illness polyneuropathy".
Endocarditis, Bacterial↗
Early terminal and nodal sprouting of motor axons after botulinum toxin.
Axonal sprouting in distal motor axons was studied in an attempt to answer two questions: (a) is the cell body required for early axonal sprouting?, and (b) do nodal, as well as terminal, axonal sprouts arise after muscle inactivity not caused by nerve injury? Botulinum toxin (BT) was used to induce axonal sprouting without nerve trauma. Mice were injected in the right calf with a sublethal dose of BT and the soleus muscle examined ultrastructurally at times varying from 3 h to 5 days post-injection. Terminal axonal sprouts were seen 2 days after injection, and based on the time taken for BT to act and the growth rate of sprouts, axons were calculated to sprout within 24 h of muscle inactivity. This short time suggests that early axonal regrowth is initiated and controlled at the distal axon. Sprouts were seen arising from the intramuscular nodes of Ranvier from 2 days after BT injection. Unlike the terminal sprouts which elongated over time, the nodal sprouts remained short and confined by the basal lamina overlying the node, probably because without structural denervation there were no empty perineural sheaths to act as pathways to the motor endplates. The finding of terminal and nodal sprouts after botulinum toxin supports the hypothesis that muscle inactivity gives rise to a single growth factor for both terminal and nodal sprouting.
Animals↗
A woman with dementia and parkinsonism unresponsive to levodopa.
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Alzheimer Disease↗
Axonal sprouting after botulinum toxin does not elicit a histological axon reaction.
In an attempt to determine which elements of the axon reaction are essential for early axonal outgrowth, axonal sprouting was induced with botulinum toxin (BoTx) and the nerve cell body changes compared with those accompanying axonal growth after nerve trauma. Anterior horn cells of mice were examined histologically at times ranging from 3 days to 3 weeks after either BoTx hindlimb injection or sciatic nerve crush. After sciatic nerve crush there was dispersion of Nissl substance, increase in cell body size, and an increase in neurofilament protein staining. None of these changes were found after BoTx-induced terminal axonal sprouting, suggesting that these morphological features of the axon reaction are not essential for early axonal outgrowth.
Animals↗
Catecholamine-secreting paragangliomas of the base of the skull. Report of two cases.
Two cases of catecholamine-secreting paragangliomas of the base of the skull are described. The patients presented with uncontrollable hypertension and, after investigation, tumors were discovered in the regions of the glomus jugulare and pterygopalatine ganglion, respectively. After cardiovascular stabilization and tumor embolization, the tumors were surgically removed, with subsequent resolution of hypertension. The incidence of these tumors is discussed.
Adult↗
Pelizaeus-Merzbacher disease in a brother and sister.
A brother and sister developed a slowly progressive neurological disorder with cerebellar and pyramidal signs and mild dementia. The brother developed symptoms at 6 months and died aged 11 years; the sister developed symptoms at 3 years and died aged 18 years. At post-mortem both had severe widespread central nervous system demyelination with islands of preserved myelin, and small amounts of sudanophilic lipid products. Metachromatic material, globoid cells, and adrenal abnormalities were not seen. The features were those of Pelizaeus-Merzbacher disease (PMD). It has been proposed, on the basis of only a few family studies, that PMD is an X-linked recessive disorder. These cases suggest that autosomal recessive inheritance may occur.
Adolescent↗
Intramedullary spinal cord metastases: a clinical and pathological study of nine cases.
The clinical and pathological findings in nine cases of intramedullary spinal cord metastases are reported and are compared with those of previous studies. Intramedullary metastases are more common than is generally believed and the incidence is probably increasing with the more prolonged survival of cancer patients. A wide spectrum of symptoms and signs may be produced, frequently with attendant diagnostic difficulties. Most patients present with myelopathy as the first manifestation of cancer or of its recurrence. Symptoms may be present for several months, with few clinical signs, despite distortion and destruction of much of the spinal cord by tumour. The extent of metastatic disease remains limited in a significant proportion of patients. No neurological symptoms or signs differentiate intramedullary metastases clearly from the more common extradural deposits. However, the diagnosis should be considered when myelopathy evolves more slowly, where plain radiographic evidence of adjacent vertebral disease is absent, and particularly when myelography is normal. Early diagnosis and aggressive medical treatment may provide for a more favourable outcome.
Aged↗
Leigh's disease: a cause of arterial hypertension.
An 11-year-old boy developed sudden and severe arterial hypertension. A post-mortem examination revealed bilateral symmetrical lesions in the medulla oblongata which were typical of Leigh's disease (subacute necrotizing encephalomyelopathy). Other cases of Leigh's disease with hypertension or left ventricular hypertrophy have shown similar brain stem lesions. Bilateral lesions of Leigh's disease in the dorsal medulla involving the solitary tract and nucleus can cause neurogenic hypertension and this may be an important clinical sign which has been neglected.
Brain Diseases, Metabolic↗
Familial visual loss and a vanishing brain tumour.
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Aged↗
Straddling Virchow's triad.
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Disseminated Intravascular Coagulation↗
Needle muscle biopsy: will it make open biopsy obsolete?
Seventy-five needle muscle biopsies have been performed in this department over the past two years. Adequate biopsies were obtained in 69 cases. In 40 cases a variety of neuromuscular conditions was seen, broadly categorised as necrotizing myopathy (10), neurogenic atrophy (7), metabolic myopathy (5), vasculitis (2), normal muscle (7), and non-specific changes (9). Twenty-nine cases were for muscular dystrophy carrier detection. There were no complications associated with the procedure. The technique is simple and quick, and can be performed on outpatients or in the ward. Needle biopsy is the method of choice for sampling skeletal muscle in most patients, although open biopsy is still indicated for certain conditions.
Adolescent↗