Biomedical subjects
I R Griffiths
Publications and source records attributed to I R Griffiths.
The Key-Gaskell syndrome: the current situation.
During the past 12 months an apparently new disease of cats has occurred with increasing frequency throughout the United Kingdom causing high morbidity and mortality and arousing considerable interest both within and outside the profession. The purpose of this paper is to report what is known about the disease and to indicate lines of current research. As there is an urgent need to communicate information it will be appreciated that this paper is incomplete in certain areas such as pathology and epidemiology where studies are still in progress.
The pathology of a sensory neuropathy affecting Long Haired Dachshund dogs.
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The relationship of glucose utilization and morphological change in the visual system in hexacarbon neuropathy.
A reduction in local glucose utilization occurs in the superficial layer of the superior colliculus of rats following exposure to 0.5% 2,5-hexanedione in drinking water for 3 weeks. Axonal pathology, with increased neurofilaments and swelling, is seen at about 5 weeks in the distal portions of the optic pathways to the superior colliculus. These lesions in the optic system occur earlier and are more marked than those in the peripheral nerves and dorsal columns. The results suggest that the functional abnormality, as implied by the decreased glucose utilization, precedes the morphological changes in hexacarbon neuropathy.
Case of isolated sensory trigeminal neuropathy in a dog.
A two-year-old rough collie bitch with a five-week history of excess salivation, coughing and dysphagia was examined. The dog had bilateral sensory loss over the whole trigeminal field while motor function of the fifth cranial nerve was preserved. No other neurological abnormalities were detected. The dog was observed over 18 months during which the condition did not progress. It was destroyed 18 months after the onset of trigeminal signs following development of a systemic illness, refractory to treatment and unrelated to the neurological signs. Pathological abnormalities were limited to the three major branches of both fifth nerves and the gasserian ganglia. There was partial loss of myelinated nerve fibres in each branch and also in the spinal tract of the fifth nerve in the brain stem. It was considered that the primary abnormality was in the gasserian ganglion and that the fibre loss was secondary to the neuronal lesion in the ganglia. The motor nucleus of the fifth nerve was normal. No cause could be found for this isolated sensory neuropathy of the trigeminal nerve.
Tumours involving the brachial plexus in seven dogs.
Seven cases with tumours localised in the brachial plexus are described. The main clinical features were a progressive lameness in one forelimb with marked muscle atrophy and very obvious but non-localizable pain. A palpable lump in the axilla was present in less than half the cases. Ancillary aids contributed little in the diagnosis except for electrophysiology which gave evidence of neural damage at an early stage of the disease and as such may be the most useful aid to an early diagnosis. Two different pathological entities were observed, the first where the tumour, primarily of neural origin (usually a neurofibrosarcoma), arose within the nerves themselves and the second where the tumours arose in adjacent tissue and involved the plexus by local infiltration. In all cases the prognosis was hopeless because of local infiltration of the tumour and metastases. In the early stages accurate diagnosis can be difficult in the absence of a mass but the possibility should be considered in any case where chronic lameness with obvious non-localizable pain is present in one forelimb.
Shaking pups: a disorder of central myelination in the spaniel dog. II. Ultrastructural observations on the white matter of the cervical spinal cord.
The ultrastructure of the cervical cord is described in a new canine mutant with severe hypomyelination of the C.N.S. Axons were either non-myelinated or surrounded by a myelin sheath that was markedly reduced in both its thickness and length of internode. Myelinated and non-myelinated zones were present on a single axon. There was no paucity of oligodendrocytes but many of those present contained empty or granular vacuoles within the cytoplasm. Features suggesting immaturity of myelination were commonly found at paranodes and along the internode. Abnormal inter-relationships of oligodendrocytes and astrocytes were present at many paranodes. These observations suggest an intrinsic defect of oligodendrocyte metabolism such that they are incapable of normal extension of their plasma membranes, while the cytoplasmic vacuoles may represent breakdown of defective lipids.
Giant axonal neuropathy: neurofilaments isolated from diseased dogs have a normal polypeptide composition.
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Shaking pups: a disorder of central myelination in the Spaniel dog. Part 1. Clinical, genetic and light-microscopical observations.
A new disorder of central myelination has been recognised in male Springer Spaniel pups which is probably inherited in a sex-linked recessive mode. The affected animals were much reduced in weight an size and showed gross generalised tremor, particularly when aroused, at about 10-12 days of age. Affected pups were studied between 1 and 3 months of age. There was severe hypomyelination throughout the CNS which was more marked in the cerebrum and optic nerves than in the spinal cord. The amount of myelin at each location increased with age. Axonal calibre also increased and there was no difference between the axonal diameters of affected and age-matched normal pups. Axons were either naked or surrounded by a disproportionately thin layer of myelin. Myelinated internodes tended to be short and heminodes were frequent. Vacuoles were present adjacent to axons or within glia but there was no evidence of demyelination. Total glial numbers were not reduced and numerous oligodendroglial and astrocytic nuclei identified. Peripheral, cranial and autonomic nerves were myelinated normally. It is suggested that there is an abnormality of oligodendroglial metabolism such that they cannot form and maintain normal myelin. Consequently the radial and longitudinal extensions of their plasma membranes are reduced. The vacuoles may represent a breakdown of defective myelin lipids as suggested in certain murine mutants. This defect of myelination provides a further model in which normal and disordered myelinogenesis can be studied.
Canine giant axonal neuropathy; some aspects of its clinical, pathological and comparative features.
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Glucose utilization in the central nervous system in the acute gliopathy due to 6-aminonicotinamide.
Sprague-Dawley rats were injected intraperitoneally with 5 mg. per kg. of 6-aminonicotinamide. The local glucose utilization rate (LGU) was measured throughout the central nervous system using the (14C) 2-deoxyglucose, quantitative autoradiographic technique at 3, 6, 12, and 24 hours after injection. The histologic appearance of selected areas of central nervous system was studied at 6, 12, and 24 hours and 3 and 10 days after injection, following perfusion by buffered aldehydes and plastic embedding. Decreases in LGU o 25 to 36 per cent were found in the lumbar ventral horn, caudal brain stem, and cerebellum at 3 and 6 hours. By 12 hours, virtually all of the structures examined showed decreases in LGU greater than 20 per cent with the reduction in the cord being 40 to 50 per cent. At 24 hours, the majority of areas exhibited definite recovery of LGU. Mild glial swelling, particularly of oligodendroglia, was noted at 12 hours and was obvious by 24 hours. Neuronal changes were not seen. These abnormalities were most marked in the intermediate and ventral gray matter of the cord and certain brain stem nuclei. 6-Aminonicotinamide has a known inhibitory effect on the pentose phosphate shunt and a secondary effect on the direct glycolytic pathway. The reduction in LGU is probably due to the inhibition of these pathways in both glia and neurons, but, the recovery LGU at 24 hours when the glial pathology was increasing suggests that the glia may metabolically protect the neuron at times of stress.
A progressive axonopathy of Boxer dogs affecting the central and peripheral nervous systems.
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The response of feline spinal pial arterioles to norepinephrine.
The effect of norepinephrine on the diameter of feline spinal pial arteries and arterioles was studied by microapplication of the drug to the perivascular environment. Vascular diameter was determined by the television image-splitting method. Application of norepinephrine over the range of 5 x 10(-8) M to 5 x 10(-3) M to spinal pial arterioles resulted in constriction of the vessels. The dose-response curve showed a tendency to plateau at concentrations above 5 x 10(-5) M, with a maximal constriction of 28.8 +/- 5.1% at 5 x 10(-3) M. The reduction in vessel diameter to microapplication of norepinephrine was prevented with the inclusion of an equimolar concentration of the alpha-adrenergic blocker, phentolamine, in the injectate. The data indicate the presence of alpha-adrenergic receptors on the smooth muscle of spinal pial arterioles, and it is suggested that the arguments pertaining to the sympathetic control of blood flow in the brain apply also to the spinal cord.
Ischaemic neuromyopathy in cats.
The effect of ischaemic neuromyopathy in cats on peripheral muscles and nerves is described. Motor function was severely decreased distal to the stifle particularly in the cranial tibial muscles. Skin sensation was absent distal to the mid tibial or hock level. The affected muscles were often hard and painful. Improvement of motor function began two to three weeks after onset and complete recovery could occur. Conduction to the interosseous and anterior tibial muscles is absent or severely reduced initially but returned and improved within two weeks. A few peripheral nerve fibres could survive the ischaemia, others showed varying defects on the myelin sheath but the majority degenerated. Shorter term recoveries were probably due to repair of the myelin sheath. Regenerated nerve fibres were also demonstrated. The cranial tibial muscles were commonly infarcted while less severe myopathic changes were found in the gastrocnemii. Provided further ischaemic episodes can be prevented the prognosis in these cases appears good.
The central nervous system in canine giant axonal neuropathy.
The pathology of the central nervous system (CNS) in a dog with giant axonal neuropathy (GAN) is presented. Swollen axons containing excessive and disorganised neurofilaments were present in the spinal cord, mainly at the distal portions of long tracts. The fasiculus gracilis and dorsal spinocerebellar tracts were affected only in the rostral cervical cord while the lateral cortico spinal tract was principally involved in the lower thoracic and lumbar cord. Occasional swellings were also found in the central dorsal columns of the rostral lumbar segments and in the dorsal and intermediate grey matter. The nuclei gracilis and cuneatus, restiform body and ventral spinocerebellar tracts were all involved in the brain stem. Spheroids were seen in the white matter of the rostral cerebellar vermis and in the granule cell layer. The brachium of the superior colliculus contained swollen axons and the cortex was diffusely involved with spheroids. The distribution was of a distal axonopathy and the cortical changes provided an explanation for the abnormal EEG and mental retardation found in some human patients.