Biomedical subjects
Publications and source records attributed to A de Lahunta.
Diffuse neuromuscular disease occurs sporadically in dogs. The most commonly reported diffuse neuromuscular diseases are polyradiculoneuritis (coonhound paralysis), tick paralysis, botulism, and myasthenia gravis (1,2,12). This clinical report describes an atypical presentation of a diffuse neuromuscular disease in a dog.
A 3-year-old horse presented with intermittent generalized seizures of 2-month duration. During interictal periods, the horse appeared normal and a cause for the seizures could not be identified. Necropsy revealed opacity of the leptomeninges, covering most of one cerebral hemisphere along with thinning and collapse of the cortex in the ipsilateral pyriform lobe. Histopathology demonstrated leptomeningeal vascular proliferation and meningothelial hyperplasia. Prominent tortuous vessels of the gyri and sulci extended into some regions of the subjacent cortex, where there was neuronal loss, ectopia, and disorganization. Clusters of prominent arterioles were found in the sclerotic choroid plexus of the lateral and fourth ventricles. Milder vascular lesions were present in the leptomeninges of the ventral brain stem, right cerebrum, spinal cord, and in the eye. The left trigeminal nerve was distorted by swollen fasicles containing onion bulb-like structures. Most bulbs contained central axons surrounded by myelin sheaths of variable thickness. Electron microscopy demonstrated concentrically arranged cells with continuous basal laminae and rare pinocytotic vesicles. S-100 immunohistochemistry showed strong positive staining in these cells. This is an unusual combination of lesions to which analogies can be drawn with the human neuroectodermal dysplasias, specifically Sturge-Weber disease. The relationship of the neuropathy to the leptomeningeal hemangiomatosis is unclear, but a compound anomaly in embryological development resulting in dysplasia and neoplasia may be involved.
Congenital portosystemic venous shunt causing signs of hepatic encephalopathy was diagnosed in 7 cats. The left gastric vein served as the shunt in four of these. Increases in blood ammonia and postprandial serum bile acids were the most consistent serum biochemical abnormalities. Excessive variation in red blood cell shape was a common but nonspecific hematologic finding. The jejunal-mesenteric venous injection of contrast material was the preferred method of portography to diagnose portosystemic shunts. Two cats were treated successfully by partial surgical occlusion of their shunts.
In the dog, the synovial cavities of the atlanto-occipital and atlanto-axial joints communicated to form a single large composite joint cavity. The prenatal development of this composite occipito-atlanto-axial joint cavity was studied by examining 26 serially sectioned dog embryos and fetuses that ranged in size from 19 to 68 mm crown-rump length, and were between 30 and 42 days of gestational age. In the composite occipito-atlanto-axial joint, trilaminar interzones developed at 19-22 mm (30-31 days), joint cavities opened at 27-32 mm (33-34 days), and the atlanto-occipital and atlanto-axial cavities first communicated at 48 mm (37 days).
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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Idiopathic feline vestibular syndrome, a peripheral vestibular deficit of unknown cause, was diagnosed in 75 cats at the New York State College of Veterinary Medicine Teaching Hospital from July 1975 to October 1984. Review of the medical records of these cats indicated that the syndrome was seen in more cats in July and August (P less than 0.001) than in other months. Clinical signs included head tilt, ataxia, rolling, rotatory or horizontal nystagmus, and occasional vomiting.
Degenerative myelopathy was diagnosed at necropsy of an adult Miniature Poodle with a 33-month history of progressive pelvic limb ataxia and proprioceptive deficit. Microscopic examination of the cord revealed diffuse degenerative myelopathy. Degenerative myelopathy is usually seen in adult, large-breed dogs and progresses over a period of months. In this case, the myelopathy progressed slowly and the degree of paralysis became more extensive than usually seen.
The serum concentration of bile acids was measured in dogs and cats with portosystemic venous anomalies (PSVA). In 14 dogs, the mean serum bile acid concentration after 12 hours of fasting was 61.7 +/- 68.7 mumol/L (normal, 2.3 +/- 0.4 mumol/L (SEM) and when measured 2 hours after a meal in 15 dogs was 229.9 +/- 87.7 mumol/L (normal, 8.3 +/- 2.2 mumol/L). The fasting serum bile acid concentration was within the normal range in 5 of 14 dogs. The postprandial concentration was determined in 3 of the 5 and in each case increased more than tenfold above the fasting value. The mean fasting serum bile acid concentration in 4 cats was 24.4 +/- 10.1 mumol/L (normal, 1.7 +/- 0.3 mumol/L) and in 2 of the cats increased to a mean of 120.6 mumol/L (normal, 8.3 +/- 0.8 mumol/L) 2 hours after feeding. The bile acid values in patients with PSVA were correlated with values for blood ammonia content, sulfobromophthalein (BSP) retention, and results of conventional tests of hepatic function. Bile acid concentrations were more sensitive than abnormalities in serum enzyme activities or BSP retention and equal in sensitivity to the ammonia tolerance test in detecting hepatobiliary insufficiency. Bile acid measurements were accomplished with less inconvenience to the patient and clinician, than tests of BSP excretion or ammonia tolerance. Used in combination with conventional laboratory tests for hepatic disease, pre- and postprandial serum bile acid concentrations appear to be a sensitive and specific indicator of hepatobiliary dysfunction of value in the diagnosis of PSVA in the dog and cat.
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.
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.
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)
Segments of peripheral nerve from dogs with canine inherited hypertrophic neuropathy ( CIHN ) were transplanted to the transected sciatic nerve of immuno incompetent mice. Regenerating mouse axons penetrated the grafts and were myelinated by dog Schwann cells. In grafts collected 3 or more months after transplantation, filamentous or granular material, identical to that occurring in nerves of affected dogs, accumulated in myelinating Schwann cells. Demyelinated fibers were only rarely found in grafted segments of affected nerve. Neither filamentous accumulations nor demyelination were observed in grafts of control canine nerve. These results indicate that CIHN is associated with a defect in Schwann cell function, and the abnormal accumulations of filaments suggest that the defect may be in the cytoskeleton. The rarity of demyelination in grafts suggests that some factor in addition to the Schwann cell defect is required to precipitate myelin destruction.
In 6 horses, clinical signs of illness implicated a lesion involving the facial and vestibulocochlear nerves. One horse had signs of otitis externa. Five horses had radiographic changes primarily involving periosteal bony proliferation of the stylohyoid bone at its articulation with the temporal bone. Five horses improved with antibiotic therapy. Otitis media-interna was found at necropsy of one horse.
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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