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Biomedical subjects

I R Griffiths

Publications and source records attributed to I R Griffiths.

141 records · Page 8Linked to original sources
PubMed1972

Some aspects of the pathology and pathogenesis of the myelopathy caused by disc protrusions in the dog.

The pathological changes in 23 cord lesions caused by disc protrusion are described. It is suggested that three broad classifications of damage can be found: (1) compressive change; (2) malacia; and (3) diffuse demyelination. The distribution of damage, within the segment, was different in each type of change as were the glial and vascular reactions. It is suggested that vascular factors play a major part in the pathology of the malacic and demyelinating lesions and may be of secondary importance in compressive lesions.

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Inherited canine giant axonal neuropathy.

To date, a single case of canine giant axonal neuropathy (GAN) has been recorded. The present report describes the disease in 3 more dogs from the second litter produced by the parents of the original case. Regular clinical and electrophysiological examinations were carried out on all 11 dogs of the second litter. At 14--16 months of age, 3 dogs developed slight posterior ataxia which progressed to a severe lower motor neuron disturbance involving only the hind legs. During this period, each dog began to regurgitate food as a result of megaesophagus. From 12 months of age, there was a progressive reduction in the amplitude of the evoked muscle action potential. Biopsy of the tibial fascicular nerve at 16 months of age confirmed that all 3 dogs had GAN, with numerous swollen unmyelinated fibers and less frequent enlarged myelinated fibers containing accumulated neurofilaments.

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A light and electron microscopic study of the neuropathy of equine idiopathic laryngeal hemiplegia.

A study has been made of the pathological changes in the recurrent laryngeal nerves from horses with clinical and sub-clinical idiopathic laryngeal hemiplegia. Qualitative and quantitative studies showed in clinical cases there was a progressive distal loss of large myelinated fibres in the left recurrent nerve. Regenerating clusters and onion bulbs were frequently seen in affected nerves both at proximal and distal levels. Degenerating axons were characterized by collections of organelles, and denervated bands of Bungner were common. Similar but less severe changes were seen in the left recurrent nerve of sub-clinical cases, and in both the clinical and sub-clinical cases the distal right recurrent nerve was also affected. Teased fibre studies showed evidence of chronic demyelination and remyelination. The aetiology of this chronic neuropathy remains uncertain but the possibility of nerve compression is discussed.

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Peripheral nervous system in a case of canine giant axonal neuropathy.

The pathology of the peripheral nerves in a dog with naturally occurring giant axonal neuropathy (GAN) is described. Axonal swellings were found predominantly in the distal portions of the tibial and recurrent laryngeal nerves. Excess neurofilaments, often arranged in whorls, were present in the swellings which were found in both myelinated and non-myelinated fibres. Other axonal organelles tended to be isolated in small pockets and on occasions adaxonal Schwann cell processes partially separated these organelles from the axoplasm. The myelin sheath was attenuated over the swellings and short lengths of demyelinated axon were often seen adjacent to the enlargements. Some Schwann cells also contained excessive microfilaments. The peripheral nerve pathology in the dog appear closely similar to that of human GAN and to certain experimental toxic neuropathies, particularly those produced by n-hexane and methyl-butyl ketone.

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Further studies of the central nervous system in canine giant axonal neuropathy.

The CNS of three further cases of canine giant axonal neuropathy (GAN) were examined. The axonal swellings were present in the distal portions of the spinal long tracts and their terminations in the cerebellar vermis; in the distal optic pathways; the nuclei of the habenulo-interpeduncular tract; certain thalamic relay nuclei and the cerebral cortex. The swellings were present both paranodally and internodally with the myelin sheath being attenuated or even absent. Excessive numbers of disordered 10 nm neurofilaments were the main constituent although mitochondria, membranous bodies, glycogen bodies and amorphous electron dense material also accumulated, particularly in the fasciculus gracilis. The neurotubules tended to form small subaxolemmal or intra-axonal islands. Complex interdigitations of oligodendroglia and axolemma were found in the affected areas. A small number of fibres in the rostral fasciculus gracilis showed marked proliferation of the smooth endoplasmic reticulum which may represent abortive attempts at regeneration. A small proportion of astrocytic processes were markedly enlarged with excessive whorling of the glial filaments. The accumulation of these various organelles in the non-terminal axon in the absence of mechanical obstruction suggests a defect in axoplasmic transport which may result from an energy failure as suggested in toxic neuropathies. The significance and pathogenesis of the glial filamentous changes and those reported in other cells in human GAN is at present uncertain.

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'Shaking pups': a disorder of central myelination in the spaniel dog. III. Quantitative aspects of glia and myelin in the spinal cord and optic nerve.

Quantification of glial cells, axonal size and myelin thickness and volume were carried out in selected areas of the three funiculi of the cervical spinal cord and the optic nerve of 'shaking pups' and normal littermates at 4 and 8 weeks of age. There was a marked reduction of oligodendrocytes in the affected pups with many of these cells having distended rough endoplasmic reticulum. Oligodendrocyte death was not noticeable. Astrocyte numbers were similar in both normal and affected pups. Axonal diameters were not reduced in the affected pups and there was no apparent correlation between myelination and axonal size in these animals. Total myelin volume and thickness were greatly reduced in the 'shaking pups.' Impaired stem cell division together with metabolic disturbance of oligodendrocytes are considered to be the main causes of the hypomyelination in this mutant.

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'Shaking pups': a disorder of central myelination in the spaniel dog. IV. Freeze-fracture electron microscopic studies of axons, oligodendrocytes and astrocytes in the spinal cord white matter.

Large axons identified in freeze-fracture replicas of the spinal cord white matter of 'shaking pups' were encircled by spiral processes at the paranodes that appeared to arise from oligodendrocytes. In the axolemma adjacent to some of these processes there were paranode-like intramembranous specializations and node-like accumulations of E-face particles; in other instances, no special contacts formed between axons and the spiral processes. The outer surfaces of the spiral processes, which often apposed astrocytes, frequently contained gap junctions. Although many of the abnormalities identified in this dysmyelinating mutant by freeze-fracture electron microscopy are probably secondary to a more fundamental defect of myelin formation, the prominence of the spiral processes suggests that the encircling of axons by oligodendrocytes may be an independent state of ensheathment and not a passive effect of myelin formation.

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Feline dysautonomia (the Key-Gaskell syndrome): an ultra structural study of autonomic ganglia and nerves.

Recently a feline dysautonomia of unknown aetiology, the Key-Gaskell syndrome, has caused widespread morbidity in the UK. This report describes the ultrastructural appearances of the autonomic ganglia and axons of the sympathetic chain in this condition. Nuclei of affected neurones were eccentric and abnormally crenated. Nucleolar abnormalities such as increased electron density (due to loss of the intranucleolar vacuoles), nucleolar segregation and ring nucleoli were observed in a proportion of neurones. There was marked loss of ribosomes, both bound and unbound, and cisternae of the rough endoplasmic reticulum were distended with a floccular electron dense material. Numerous smooth-walled cisternae were also present and complex stacks of smooth semi-parallel membranes were observed, probably derived from the smooth endoplasmic reticulum or Golgi apparatus. No normal Golgi formations were seen. Frequent autophagic vacuoles and membranous dense bodies were present in some cells. Many unmyelinated fibres in the sympathetic chain were swollen and contained vesiculo-tubular profiles, disordered neurotubules and filaments and various degenerating membranous organelles. Myelinated fibres within the sympathetic chain were also degenerating. These studies indicate that the organelles involved with protein biosynthesis are severely affected by the disease.

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Progressive axonopathy: an inherited neuropathy of boxer dogs. 2. The nature and distribution of the pathological changes.

This report describes the neuropathology of progressive axonopathy (PA), an autosomal recessive inherited neuropathy of Boxer dogs, which affects CNS and PNS. The nerve roots contain numerous myelin bubbles and proximal paranodal axonal swellings containing vesicles, vesiculo-tubular profiles and disorganized neurofilaments. The myelin sheath overlying such swellings is often attenuated. As the disease develops there are progressive changes in the myelin sheath with thinning at paranodal and internodal locations, loss of myelin from lengths of axon and the formation of short internodes with disproportionately thin sheaths. The abnormalities show a very definite selectivity for nerve roots and proximal nerves. Conversely, the frequency of degeneration and regeneration is greater distally except in the cervical ventral roots which contain numerous regenerating clusters. In the CNS numerous axonal spheroids are found in the lateral and ventral columns of the spinal cord and in various brain stem nuclei, particularly the superior olives, accessory cuneate nuclei and lateral lemniscus and its nucleus. Axonal degeneration which occurs mainly in the cord shows no obvious tract or proximal/distal selectivity. The optic pathways are also involved, predominantly adjacent to the chiasma. The autonomic nervous system is affected and distal limb muscles show varying, but usually minor, degrees of neurogenic atrophy. The condition, which has no obvious direct parallel in human or veterinary medicine, shows gross disturbances of axon-glial inter-relationships in both CNS and PNS.

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Progressive axonopathy: an inherited neuropathy of boxer dogs. An immunocytochemical study of the axonal cytoskeleton.

The distribution of the major axonal cytoskeletal proteins has been determined in lumbar ventral roots and spinal cord of dogs with progressive axonopathy, an inherited neuropathy of boxer dogs. The three neurofilament proteins, and beta-tubulin, actin and fodrin were localized using immunocytochemistry. The majority of swollen axons in the nerve roots contained excessive, disorientated neurofilaments. In about 5% of such fibres the peripheral filaments in the axoplasm were orientated circumferentially and such zones were deficient in tubulin. Many, but not all, spheroids contained increased amounts of actin, often with internal areas of more intense staining. Similar findings were present in axonal swellings in the CNS, although their contents were more variable. The distribution of axonal fodrin in CNS and PNS appeared unaltered. The perikarya of many motor neurons in the spinal cord and brain stem contained phosphorylated neurofilaments. The results support previous suggestions that defects in slow axonal transport are involved in the pathogenesis of this disease.

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