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Biomedical subjects

J F Cummings

Publications and source records attributed to J F Cummings.

At least 73 records · Page 4Linked to original sources
PubMed1988

A study of cerebellar and cerebral cortical degeneration in miniature poodle pups with emphasis on the ultrastructure of Purkinje cell changes.

In a litter of three Miniature Poodles, a normal female pup contrasted with two males which displayed severe equilibrium and postural disturbances soon after birth. In the male pups diffuse cerebral cortical degeneration accompanied cerebellar cortical atrophy, which was characterized by extensive loss and degeneration of Purkinje neurons. As in some prior histological descriptions of canine cerebellar atrophies, degenerating Purkinje cells appeared either pale, swollen and vacuolated or shrunken and hyperchromatic. Swollen vacuolated cell bodies and condensed necrotic neurons were scattered through the cerebral cortex. Ultrastructural studies revealed that the vacuolar degeneration in Purkinje and cerebral neurons was referable to marked dilation of endoplasmic reticulum and loss of ribosomes. In shrunken Purkinje neurons, increased cytoplasmic eosinophilia was associated with a decline in Nissl bodies and accumulations of mitochondria and especially lamellar bodies. The latter, stacked derivatives of endoplasmic reticulum, were not encountered in shrunken cerebral perikarya. Lamellar bodies reached giant proportions in the dendritic stems of degenerating Purkinje neurons. In Purkinje axons, however, these bodies often were overshadowed by aggregates of axoplasmic tubules. The cytological changes in these Poodle pups were notably different from those reported in earlier ultrastructural studies of canine inherited cerebellar degenerations.

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PubMed1988

Attempts to prevent equine post neurectomy neuroma formation through retrograde transport of two neurotoxins, doxorubicin and ricin.

Digital neurectomies, performed to relieve pain and lameness, are often complicated postoperatively by formation of painful neuromas. In this study attempts were made to deliver lethal doses of neurotoxin to the cell bodies of the transected digital nerve fibres via long-distance retrograde axon transport and, thereby, prevent the regenerative changes that lead to neuroma formation. After applying doxorubicin in various ways to the digital nerve stumps of ponies, degenerating or necrotic neurones appeared only sporadically in the spinal ganglia. Although doxorubicin was largely ineffective in retrograde destruction of cell bodies, when absorbed in pledgets on the stumps it exerted a sustained action which prevented Schwann cell proliferation and axon sprouting. Ricin, in contrast to doxorubicin, was effective in retrograde destruction of sensory neurons. Many affected neurons were devoid of polysomes but packed with mitochondria; others had advanced to various stages in cytolysis. Despite its effectiveness, ricin cannot be recommended because of its extreme toxicity. The clinical use of retrograde transport in equine neurectomy will probably depend on future development of hybrid toxins with high neural specificity and low systemic toxicity.

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PubMed1988

Multisystemic chromatolytic neuronal degeneration in a Cairn terrier pup.

In a four-month-old female Cairn terrier with mild episodic paraparesis, a multisystemic chromatolytic degeneration affected widespread neuronal populations in the brain and spinal cord as well as spinal, autonomic, and enteric ganglia. There was little axon degeneration or cell body loss, and the latter findings may explain the mild clinical signs. Among affected perikarya the extent and distribution of chromatolysis varied. While peripheral lysis of Nissl substance occurred often in spinal motoneurons, central chromatolysis was frequent in brain stem nuclei, and patchy Nissl loss appeared in some neurons including those in the cerebral cortex and spinal dorsal horns. Although prior studies of various chromatolytic neurodegenerations often have demonstrated characteristic massings of neurofilaments, the major, and invariable ultrastructural finding in this study was dispersion and loss of ribosomes. Neurofilamentous accumulations were observed less consistently. The clinical and pathologic findings in this pup were compared and constrasted with those made in prior studies of chromatolytic neurodegenerations.

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PubMed1986

Tremors in Samoyed pups with oligodendrocyte deficiencies and hypomyelination.

Over a 3-year period a breeder of Samoyed dogs observed six litters in which one or more pups at 3 weeks of age showed generalized tremors and an inability to stand. One affected pup, a 5-week-old male, was referred for clinical and pathological evaluation. Gross and microscopic studies including immunocytochemical demonstration of myelin basic protein, revealed a lack of myelin throughout the central nervous system. Ultrastructural studies revealed that a total absence of normal myelin was associated with oligodendroglial deficiencies. Oligodendrocytes were immature in appearance, greatly reduced in number, and incapable of forming compact myelin. Astrocytosis and an increase in the third type of neuroglial cells were observed. The changes differed from those reported in other canine forms of hypomyelinogenesis and were compared with hypomyelinating diseases in other species. The findings suggested that this hypomyelination was the result of retarded gliogenesis.

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PubMed1986

Progressive muscular dystrophy in a golden retriever dog: light microscope and ultrastructural features at 4 and 8 months.

The clinical and morphological features of a congenital myopathy in a young male golden retriever dog were studied. Muscle biopsies at 4 and 8 months of age were examined with light and electron microscopy. Clinical features included early onset of generalized muscle weakness with selective muscle atrophy and hypertrophy, splaying of the limbs, stiff gait, and marked elevation of serum creatine kinase (CK). An electromyograph revealed spontaneous electrical activity characterized by sustained high-frequency activity, which was not abolished by neuromuscular blockade. Morphologically there was marked hypercontraction and segmental necrosis of muscle fibers with phagocytosis and regeneration. Ultrastructurally, dilatation of sarcoplasmic reticulum was the most consistent feature associated with early fiber degeneration. No abnormalities were noted in the central or peripheral nervous system. Progression of the disease was evident at 8 months. It was concluded that the findings are consistent with a dystrophic process of primary muscle origin. The probable genetics and comparison to other animal models of muscular dystrophy and to Duchenne dystrophy are discussed.

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PubMed1985

The origins of innervation of the esophagus of the dog.

This study defined the origins of extrinsic efferent and afferent innervation of the normal canine esophagus. When all the layers of the wall of the 3 esophageal regions (cervical, thoracic and abdominal) were injected with horseradish peroxidase (HRP), labeled nerve cells were found in the nucleus ambiguus (NA) and parasympathetic nucleus of X (PX) of the brainstem. Most labeled cells in the NA were located in the compact column (retrofacial nucleus) while labeled cells in the PX were located in separate rostral and caudal areas. There was no somatotopic organization in either the NA or PX. Labeled sympathetic postganglionic neurons were found in the cranial cervical, middle cervical, cervicothoracic, thoracic sympathetic trunk and celiacomesenteric ganglia. The HRP injection of the esophageal wall labeled sensory cell bodies in the glossopharyngeal, proximal and distal vagal, and C2-T6 spinal ganglia. There was no discernible pattern of distribution of labeled cells in the autonomic or sensory ganglia. When the HRP injections were confined to the mucosa-submucosa layers of the thoracic esophagus, a small number of labeled cells were identified in the NA; however, no labeled cells were found in the NA when injections were confined to the mucosa-submucosa of either the cervical or abdominal esophageal regions. With these confined injections, the labeled nerve cells appeared in the rostral part of the PX. Thus, it appeared that the internal tunics of the esophagus (i.e., the mucosa and submucosa) were innervated by neurons in the rostral PX while the muscular tunic was innervated by neurons in the caudal PX and the rostral NA. After mucosa-submucosa injections, labeled sympathetic neurons appeared in the same ganglia that were identified after whole wall injections and these had a similar random distribution. These injections also labeled neurons in the glossopharyngeal, proximal vagal, and distal vagal ganglia, but unlike the whole wall injections there was no labeling in the spinal ganglia. This suggested that the labeled cells of the spinal ganglia seen after whole wall injections conveyed impulses from the tunica muscularis and serosa.

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PubMed1985

GM2 gangliosidosis in a Japanese spaniel.

A storage disease in a 2-year-old Japanese Spaniel resembled a GM2 gangliosidosis previously identified in a now extinct line of German Shorthaired Pointers. Despite a later appearance of signs in the Japanese Spaniel, the distribution, staining, and ultrastructure of the stored material were similar in the two breeds. Golgi studies of cerebral cortical neurons revealed the formation of spiny and aspiny enlargements at the axon hillock region (meganeurites) and the growth of secondary neurites from this region. As in the German Shorthaired Pointer model, there was massive storage of GM2 ganglioside as well as a seemingly paradoxical increase in total beta-hexosaminidase activity measured in vitro.

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PubMed1985

Distribution of substance P-like immunoreactivity in the enteric neurons of the large colon of normal and amitraz-treated ponies: an immunocytochemical study.

The distribution of the putative motor excitatory neurotransmitter, substance P, was studied immunocytochemically in the left dorsal colon of four normal control ponies and three ponies with amitraz-induced impaction colic. Substance P-like immunoreactivity in the control ponies was observed in nerve fibres in all layers of the bowel wall and in the nerve cell bodies of the enteric ganglia. The substance P-like immunoreactivity was clearly more intense in the cell bodies of submucosal ganglia than in those of the myenteric ganglia. The internodal nerve strands of the myenteric plexus were very rich in substance P-like immunoreactivity and within the ganglia they formed dense varicose networks around the neuronal cell bodies. Nerve bundles rich in substance P-like immunoreactivity diverged inward from the myenteric plexus to contribute an abundance of varicose immunoreactive fibres to the circular muscle of the tunica muscularis. Nerve fascicles with substance P-like immunoreactivity were sparse in the longitudinal muscle except in the thickened taenial band. In the submucosa many of the nerve fibres with substance P-like immunoreactivity appeared to arise from ganglionic cell bodies. Immunoreactive fibres commonly condensed around arterial vessels in the submucosa. Fine immunoreactive nerve fascicles from the submucosal plexus also projected internally to supply the muscularis mucosae and form periglandular arrays in the lamina propria. The distribution of substance P-like immunoreactivity in the normal equine colon differed in some respects from patterns observed in large intestines of other mammals. When the colons of normal and amitraz-treated ponies were compared no differences were discerned in the distribution or intensity of substance P-like reactivity.

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PubMed1985

Preliminary studies on long distance, retrograde transport of horseradish peroxidase in equine peripheral nerves.

As a prelude to studies on retrograde axonal transport of neurotoxin (ie, so-called suicide transport) as a means to prevent post neurectomy neuroma formation, preliminary studies were conducted with an innocuous enzymatic marker, horseradish peroxidase (HRP). The proximal stumps of resected medial and lateral palmar digital nerves in six ponies were injected via a tuberculin syringe and needle with 50 micron 1 of a 30 per cent solution of HRP in order to assess long distance retrograde axonal transport. The dorsal root ganglion of the cervical spinal enlargement (ie, C6, C7, C8, T1, T2) were removed at post injection intervals of two, four, six, eight, 10 and 12 days. These were sectioned serially and reacted by the tetramethylbenzidine method to demonstrate transported enzyme in the ganglionic cell bodies which give rise to sensory fibres of the palmar digital nerves. Enzyme, retrogradely transported over axon lengths of 115 cm, was first demonstrated in spinal ganglia four days after injections of the palmar digital nerves. The calculated transport velocity of 287 mm/day, although almost certainly an underestimate, greatly exceeded rates of 72 to 120 mm/day recorded previously with HRP in the peripheral nerves of small laboratory animals. The intensity of the HRP reaction product in ganglionic neurons was strong at four days and it remained unabated in ganglia examined at six, eight, 10 and 12 days post injection. The major sources of the sensory fibres of the palmar digital nerves appeared to be the ganglia of the C8 and T1 spinal segments which contained more than 90 per cent of all labelled neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1985

Trials of serotonin, substance P and alpha 2-adrenergic receptor effects on the equine large colon.

Some support for both serotonin and substance P as biotransmitters in the equine large colon is presented. Close arterial injections of small quantities of each of these were effective, respectively, in stimulating marked increases in coordinated pressure peaks in the vicinity of the pelvic flexure, with modest (serotonin) or marked (substance P) increase in colon artery blood flow. Both the acaricide, amitraz, and the tranquilizer xylazine appeared to act on the equine large colon via yohimbine-sensitive alpha 2-adrenergic receptors.

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PubMed1985

Presumptive organophosphate-induced delayed neurotoxicity in a paralyzed bull.

A case of presumptive organophosphate-induced delayed neurotoxicity in a bull is described. All signs were referable to a focal cervical or diffuse spinal cord lesion. These included recumbency with severe symmetrical paresis of all 4 limbs, the hind limb involvement being greater than the forelimbs. CSF analysis was normal. The bull was killed and necropsied. There were no gross CNS lesions. Histopathologic finds are characterized and their resemblance to lesions observed in delayed neurotoxicity caused by organophosphate compounds is discussed. The bull had been treated with organophosphate insecticide (famphur) 43 days prior to the onset of signs.

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PubMed1985

Progressive paresis in sheep due to delayed neurotoxicity of triaryl phosphates.

This report describes the history, signs, histopathology, and diagnosis of a delayed neurotoxicity in Suffolk sheep caused by transmission oil. The signs of toxicity included hyperexcitability, a stiff gait, tetraparesis and inability to maintain sternal recumbency. The circumstances involved in exposure to the transmission oil were determined. Histopathology revealed widespread degeneration of axons in the spinal cord, especially their more distal portions.

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PubMed1984

Reduced substance P-like immunoreactivity in hereditary sensory neuropathy of pointer dogs.

Two unrelated Pointer dogs, each from a breeding of normal parents which produced three affected pups in a litter of nine, began to bite their paws at 3 and 5 months of age. Insensitivity to painful stimuli was marked in the distal parts of the limbs and receded proximally. The affected dogs were euthanatized at 5 and 20 months because of acral mutilation and infection. Changes affecting the primary sensory neurons included: small spinal ganglia with reduced numbers of cell bodies, degeneration of unmyelinated and myelinated fibers in dorsal roots and peripheral nerves, and reduced fiber density in the dorsolateral fasciculus (dlf). Since nociceptive loss was the salient deficit in a neuropathy affecting primary sensory neurons, immunohistochemical studies focused on substance P, the undecapeptide imputed to mediate nociception at the first synapse in the spinal cord and brain. The localization and density of substance P-like (SPL) immunoreactivity was studied in three control dogs and the two Pointers by the indirect antibody peroxidase-antiperoxidase method. The spinal intumescences of the control dogs contained dense SPL-immunoreactivity in fibers of the dlf and the superficial laminae of the dorsal horn (i.e., laminae I, II, and the dorsal part of III). Immunoreactive fascicles on the lateral aspect of the dorsal horn and in the reticular process sent contributions medially to a plexiform fiber arrangement in lamina V. Medially, SPL-immunoreactive fibers were more loosely arranged in the internal third of laminae VI and VII and in lamina X.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1984

Canine inherited hypertrophic neuropathy: clinical and electrodiagnostic studies.

Clinical and electrodiagnostic features of acute and chronic canine-inherited hypertrophic neuropathy were studied in 20 affected dogs. The age of onset was consistently between 7.5 and 10 weeks of age. Affected pups had rapidly developing limb weakness accompanied by muscle hypotonia and hyporeflexia. There was no clinical evidence of cranial nerve dysfunction. Pups that did not develop limb contractures later regained some strength and became clinically stable for long periods, although they always remained weak. Progressive slowing of nerve conduction velocities occurred during the development of clinical signs of limb weakness. Temporal dispersion of evoked muscle action potentials was present in more chronically affected dogs. Transient spontaneous activity was present in muscles of affected dogs examined by electromyography. An autosomal recessive mode of inheritance was supported by the results of breeding studies.

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PubMed1983

Ganglioradiculitis in the dog. A clinical, light- and electron-microscopic study.

Facial hypalgesia, sensory ataxia, depression of tendon reflexes, and masticatory muscle wasting developed acutely to subacutely in three adult dogs. These deficits were correlated with craniospinal sensory ganglioradiculitis. CNS degeneration in the dorsal funiculus, spinal tract of the trigeminal nerve, and solitary tract was secondary to loss of primary sensory neurons. Megaesophagus, which occurred in two dogs appeared to be associated with loss of vagal primary afferent neurons; however, esophageal and gastric myenteric ganglionitis was also observed in one of these animals. In the three dogs changes in the sensory ganglia and roots included non-suppurative inflammation and degeneration and loss of neurons. Perivenular and perineuronal mononuclear infiltrates were prominent. EM study revealed that the satellite cells around degenerating and necrotic cell bodies were commonly invaded and displaced by lymphocytes and macrophages. It was not clear whether these mononuclear cells effected neuronal degeneration or merely responded to it. Although the pathogenesis remained undefined, the similarity of the clinical and pathologic findings in these dogs indicated a nosologic entity that had not been reported previously. This canine ganglioradiculitis was compared with inflammatory disorders of the cranial and spinal ganglia in man.

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