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PubMedDate not supplied

Complications and long-term results after partial laryngectomy for the treatment of idiopathic laryngeal paralysis in 45 dogs.

Forty-five dogs with severe respiratory signs caused by idiopathic, acquired laryngeal paralysis were treated by partial laryngectomy. The predominant postoperative complications were coughing in 28 dogs and pneumonia in 15 dogs. Eight dogs required a second operation to alleviate persistent or recurrent upper airway obstruction. Results of surgery were considered excellent in 11 dogs (25%), good in 18 dogs (40%), fair in 6 dogs (13%), and poor in 10 dogs (22%). Poorer results were obtained by surgical residents than by more experienced surgeons. Death in the immediate postoperative period was related to pneumonia (8 dogs) and laryngeal collapse (1 dog). Nine dogs died later of respiratory disease. Although partial laryngectomy is effective for the treatment of laryngeal paralysis, it is not recommended because of the high incidence of postoperative complications.

Airway Obstruction↗
PubMed2002

Transient post-traumatic hemidiaphragmatic paralysis in two cats.

A diagnosis of post-traumatic hemidiaphragmatic paralysis was made in two cats. Both cats had a history of trauma and paradoxical inward movement of the abdominal wall at inspiration. Thoracic radiographs were taken at inspiration and expiration. Although the images were suggestive of hemidiaphragmatic paralysis, definitive diagnosis was reached by fluoroscopy in one cat and by ultrasonography in the second. Both cases resolved spontaneously and diaphragmatic function was normal at follow-up.

Animals↗
PubMed1977

Vestibular disease, and its relationship to facial paralysis in the horse: a clinical study of 7 cases.

The signs observed in 6 cases of peripheral vestibular disease included incoordination, head tilt and nystagmus. The intensity of the signs varied greatly with duration of the disease, and in 3 cases facial paralysis was also present. Tympanosclerosis was demonstrable in all cases subject to radiology. Trauma was the causative factor in most cases. The causes of, and relationships between, vestibular dysfunction and concomitant facial paralysis are discussed. The exact etiology of the tympanosclerosis is unknown.

Animals↗
PubMed1987

Infestation in the dog by the paralysis tick Ixodes holocyclus. 3. Respiratory effects.

To assess respiratory function in dogs with tick paralysis, respiratory measurements were recorded on 14 dogs experimentally infested with Ixodes holocyclus. There was a progressive fall in respiratory rate with no change in tidal volume, which resulted in a significant fall in minute respiratory volume in the latter stages of the disease. The fall in respiratory rate was possibly central in origin and was accompanied by an increased alveolar-arterial oxygen tension difference, probably caused by pulmonary congestion and oedema. The "grunting" respiration seen in tick paralysis was due to closure of the vocal cords during expiration and could represent an attempt to re-expand collapsed parts of the lung.

Animals↗
PubMed2003

A retrospective study of unilateral arytenoid lateralisation in the treatment of laryngeal paralysis in 100 dogs (1992-2000).

OBJECTIVE: To determine the effectiveness of unilateral arytenoid lateralisation as a surgical treatment for laryngeal paralysis in dogs. DESIGN: The case records of 100 dogs that received a unilateral arytenoid lateralisation for laryngeal paralysis between 1992 and 2000 were reviewed. The results of questionnaires on surgical outcome, formulated for the animal owner and the referring veterinarian, were analysed. Information obtained for dogs under 10 kg and dogs over 10 kg was analysed separately. RESULTS: The Labrador Retriever was the most commonly affected breed. The male:female ratio was 1.56:1 and the average age of presentation was 9.9 years. The most common month in which surgery was performed was October. The majority of owners (87.7%) felt that their dog's quality of life was improved in the 6 months after surgery. Thirty-three percent of dogs revisited the referring clinic with a respiratory problem following unilateral arytenoid lateralisation, and 10.7% of dogs were reported as having a post-surgical complication associated with the procedure. Following surgery, dogs under 10 kg revisited the referring veterinarian with a respiratory complication more often than dogs over 10 kg. Significantly fewer owners of dogs under 10 kg than owners of dogs over 10 kg felt that their dogs quality of life was improved by surgery (55% versus 93%). CONCLUSION: The majority of owners surveyed reported that unilateral arytenoid lateralisation had improved the quality of their dog's life during the first 6 postoperative months. Owner dissatisfaction with the results of surgery and the reported rate of re-presentation (for respiratory disease) may be higher for small (< 10 kg) dogs. A prospective study comparing the results of unilateral arytenoid lateralisation surgery in large and small dogs may be worthwhile in the future.

Animals↗
PubMedDate not supplied

Laryngeal paralysis-polyneuropathy complex in young Rottweilers.

Five Rottweiler puppies from 3 unrelated litters developed inspiratory stridor at 11-13 weeks of age. Physical examination disclosed tetraparesis in all dogs, and bilateral lenticular cataracts in 4 dogs. Laryngeal examination under light anesthesia showed laryngeal paralysis in all dogs. Electrodiagnostic testing revealed denervation potentials in the distal appendicular muscles of 4 dogs tested and in the intrinsic laryngeal muscles of 2 dogs tested. Motor nerve conduction velocity was slightly low in 1 dog. Neurogenic muscular atrophy was found in distal appendicular muscles (n = 3) and intrinsic laryngeal muscles (n = 2), and degenerative changes were found in peripheral nerves (n = 3) and recurrent laryngeal nerves (n = 2). No abnormalities were detected in the spinal cord, spinal nerve roots, or ganglia of 3 dogs autopsied. The clinical, electrophysiologic, and histopathologic findings support a diagnosis of polyneuropathy and resemble the finding reported in young Dalmatians. Young dogs with laryngeal paralysis should be evaluated neurologically to rule out a more generalized polyneuropathy. The condition is suspected to be hereditary in nature and the prognosis is poor.

Animals↗
PubMed1980

Pathological observations on an outbreak of paralysis in broodmares.

A description is given of the pathological changes present in 8 mares which died or were euthanased in the course of an outbreak of paralysis on a Thoroughbred studfarm. In all cases the principal changes were in the central nervous system (CNS) and consisted of a severe and widespread vaculitis in the brain, cord, sheaths of nerves, capsules of ganglia and occasionally elsewhere in the body. Associated with the damage to vessel walls there was haemorrhage and exudation of plasma into the perivascular tissues. Involvement of neurones was minimal and no neuronophagia was present. Six cases had malacic foci in the brain, related to thrombosis of local arteries. Acinar necrosis in the mammary gland was present in one case. Examinations of the CNS and cerebrospinal fluid (CSF) for the presence of equid herpesvirus 1 (EHV1) or other microbial agents proved negative but EHV1 was isolated from the spleen of one mare and from the pharyngeal mucos membrane in another. The pathogenesis of this type of paralysis is discussed.

Animals↗
PubMed1985

Bilateral laryngeal paralysis in the horse.

Four two-year-old Thoroughbreds suffered an acute gastrointestinal illness shortly after dosing with mineral oil which was thought to have been contaminated with an organophosphate compound. Three weeks later all four were noted to be dyspnoeic and endoscopic examination showed that they had developed bilateral laryngeal paralysis. Two of the horses died during severe bouts of dyspnoea six and eight months later and the third was killed shortly thereafter. Examination of the left and right recurrent laryngeal nerves from these horses showed a severe loss of myelinated fibres distally, especially in the left nerve. A similar but less severe lesion was seen in other long peripheral nerves, including the phrenic and digital nerves of the third horse. The spinal cord in two horses showed evidence of mild axonal degeneration which was not related to a particular tract or location. The fourth horse had bilateral laryngeal paralysis two years later. The acute clinical signs and delayed neurological sequelae seen in these horses were strongly suggestive of accidental organophosphate toxicity.

Animals↗
PubMed1984

Isolation of paralysis-inducing murine leukemia viruses from Friend virus passaged in rats.

Four clones of murine leukemia viruses (PVC-111, PVC-211, PVC-321, and PVC-441) were isolated from a paralyzed Fischer rat which had been infected with rat-passaged Friend leukemia virus. PVC-211 and PVC-321 viruses induced hind leg paralysis in rats and killed them within 1 month, and PVC-441 did so within 2 months after infection, whereas PVC-111 did not within 4 months. PVC-321 and PVC-441 but not PVC-111 virus grew well in brain and spinal cord media. The viral antigens were found often in glia cells and rarely in neurons of the rats infected with each of these PVC viruses. All of the PVC viruses induced neuronal degeneration but neither inflammation nor leukemic infiltration in the spinal cord. The isolated viruses were all ecotropic and NB-tropic. Age dependency of the susceptibility of rats to paralysis induction was observed.

Animals↗
PubMed1987

Monoclonal anti-I-A antibody reverses chronic paralysis and demyelination in Theiler's virus-infected mice: critical importance of timing of treatment.

Susceptibility to demyelination caused by the WW isolate of Theiler's murine encephalomyelitis viruses is linked to class II genes of the major histocompatibility complex. SJL/J (H-2s) mice, expressing only I-As class II gene products of the major histocompatibility complex, are highly susceptible to Theiler's murine encephalomyelitis virus infection with the WW virus isolate, with chronic paralysis and severe inflammation and demyelination in the central nervous system. The effect of in vivo administration of anti-I-As monoclonal antibodies on Theiler's murine encephalomyelitis virus infection was observed. SJL/J mice were treated in various protocols pre- or postinfection. Anti-I-As monoclonal antibody reversed chronic paralysis and reduced inflammation and demyelination when given after the establishment of persistent infection. The effect was long lasting, but clinical signs, inflammation, and demyelination recurred 2 months after treatment ceased. Anti-I-As antibodies had no effect on viral titers within the central nervous system. The timing of the administration of monoclonal antibodies was critical. Administration of anti-I-As before the establishment of the persistent infection resulted in fatal encephalitis.

Animals↗
PubMed1992

ts1, a temperature-sensitive mutant of Moloney murine leukemia virus TB, can infect both CD4+ and CD8+ T cells but requires CD4+ T cells in order to cause paralysis and immunodeficiency.

When neonatal FVB/N mice were inoculated with ts1, a temperature-sensitive mutant of Moloney murine leukemia virus TB, they developed a progressive bilateral hindlimb paralysis and immunodeficiency leading to death 4 to 6 weeks after inoculation. T lymphocytes have been shown to be primarily responsible for this ts1-induced syndrome. Here we compare the role played by each subset of T lymphocytes, i.e., CD4+ and CD8+ T cells, in disease development. Mice were depleted of a specific subset for the first 10 days of their lives by using either anti-CD4 or anti-CD8 monoclonal antibodies in vivo. Disease development in these mice was then monitored. Depletion of CD4+ T cells significantly attenuated the ts1-induced syndrome: virus replication was decreased, disease latency was extended, and death was prevented in 60% of the mice. Similar treatment with anti-CD8 antibody had almost no effect on disease progression. However, when depletion was begun 2 weeks after neonatal ts1 inoculation, CD4+ T cell depletion did not affect disease development. ts1 infected CD4+ and CD8+ T lymphocytes equally well in vivo, as shown by flow cytometric analysis, but virus replication was restricted primarily to the CD4+ subset of T cells, as found by in vitro assay. Hence, CD4+ T lymphocytes play an important role in the development of ts1-induced paralysis and immunodeficiency. The mechanism of this CD4+ T-cell-mediated disease production by ts1 is not clear; however, increased replication of ts1 in the CD4+ T cells, especially in the early stages of the disease, seems to play a crucial role.

Animals↗
PubMed1992

Rabies virus neuritic paralysis: immunopathogenesis of nonfatal paralytic rabies.

Two pathogenetically distinct disease manifestations are distinguished in a murine model of primary rabies virus infection with the Evelyn-Rokitnicky-Abelseth strain, rabies virus neuritic paralysis (RVNP) and fatal encephalopathogenic rabies. RVNP develops with high incidence in immunocompetent mice after intraplantar infection as a flaccid paralysis restricted to the infected limb. The histopathologic correlate of this monoplegia is a degeneration of the myelinated motor neurons of the peripheral nerve involved. While, in this model, fatal encephalopathogenic rabies develops only after depletion of the CD4 subset of T lymphocytes and without contribution of the CD8 subset, RVNP is identified as an immunopathological process in which both the CD4 and CD8 subsets of T lymphocytes are critically implicated.

Animals↗
PubMed1985

Diaphragmatic paralysis due to spinal muscular atrophy. An unrecognised cause of respiratory failure in infancy?

An unusual form of spinal muscular atrophy presenting with respiratory failure was observed in four infants from two families. In one, whose death was attributed to pneumonia, the diagnosis was inferred retrospectively after two siblings died from an identical illness and were shown to have diaphragmatic paralysis and the typical electrophysiological and histological features of spinal muscular atrophy. Other signs of skeletal muscular weakness were absent or inconspicuous. The fourth, unrelated infant presented in an identical way but has survived for over a year on a ventilator. Two months after the onset of respiratory paralysis, more extensive skeletal muscular weakness was seen. Other infants, dying of unexplained respiratory illness, may have this disorder and some may be included in the miscellany of disorders that constitute the sudden infant death syndrome.

Female↗
PubMed1985

Ultrasound monitoring of diaphragm activity in bilateral diaphragmatic paralysis.

Recovery of diaphragm activity after bilateral diaphragmatic paralysis was monitored in a term infant using a mechanical sector scanner fitted with a 5 MHz transducer. The ratio of diaphragmatic excursion during spontaneous breathing and ventilator assistance was used an objective measure for comparison of diaphragmatic activity during recovery. Ultrasound assessment of diaphragm contraction may be used to study progress in diaphragmatic paralysis.

Diaphragm↗
PubMed1986

Successful rehabilitation in conversion paralysis.

A rehabilitation programme for patients with conversion paralysis has been introduced in which they are offered physical rehabilitation. During an eight month period between October 1984 and May 1985 six patients who had been diagnosed as dependent on wheelchairs owing to conversion paralysis for a mean of 3 years (range 1-6 years) were entered into the inpatient neurorehabilitation programme. All six patients were able to walk within a mean of 41 days (range 10-70 days), and then relinquished a variety of aids and allowances as a result of their regained mobility. They continued to be independent at outpatient review for a mean of 10 months (range 8-15 months). Successful rehabilitation from wheelchair dependency can be achieved by a cost effective, prolonged, inpatient neurorehabilitation programme.

Adolescent↗
PubMed2003

Thyrotoxic periodic paralysis: an unusual presentation of weakness.

Thyrotoxic periodic paralysis is a rare endocrine disorder seen predominantly in men of Asian origin. The case is reported of a patient who presented to the accident and emergency department with sudden onset of weakness of his lower limbs. Hypokalaemia was identified and treated with resolution of symptoms. Additional tests identified the patient as being thyrotoxic. He was treated with oral antithyroid drugs. It is important to consider the diagnosis of thyrotoxic periodic paralysis in patients presenting with acute onset of weakness. The report discusses the epidemiology, presentation, treatment, and complications of this condition.

Adult↗
PubMed1983

Wildervanck's syndrome with bilateral subluxation of lens and facial paralysis.

A 15-year-old female was found to have the typical features of Wildervanck's syndrome, including Klippel-Feil anomaly, abducens paralysis, retraction of the bulbi, and deafness. In addition, she had bilateral lens subluxation and facial paralysis, neither of which have been reported in patients with Wildervanck's syndrome.

Abducens Nerve↗
PubMed1992

Unilateral diaphragmatic paralysis: an electrophysiological study.

An electrophysiological study was carried out on four patients with unilateral diaphragmatic paralysis. Whereas neurogenic involvement of the paralysed hemidiaphragm was roughly similar in all cases, neurogenic patterns could be detected in the normally moving contralateral hemidiaphragm in three cases, and the degree of involvement could be correlated with the respiratory state of the patients. EMG also showed that the neuropathic process affected the limb muscles. Thus unilateral diaphragmatic paralysis may be, at least in some cases, the localised expression of a more diffuse neuropathy, perhaps a peculiar form of neuralgic amyotrophy.

Adult↗