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Management of acute neuromuscular paralysis.

The diagnosis of acute neuromuscular paralysis includes central nervous system disorders, peripheral neuropathy, neuromuscular conduction block and muscle disease. Identification of the cause is largely a clinical problem but neurophysiological investigations are often essential and a few specific tests are helpful. The commonest cause is Guillain-Barré syndrome. Special precautions, especially monitoring vital capacity, must be taken to detect respiratory failure and avoid atelectasis and chest infection. In acute neuropathy there is an additional danger of cardiac arrhythmias which requires continuous electrocardiographic monitoring. Prolonged artificial ventilation should be supervised by a specialist multidisciplinary intensive care team. Specific treatment depends on the diagnosis: for Guillain-Barré syndrome, intravenous immunoglobulin is preferred to plasma exchange on the basis of similar efficacy but greater convenience; steroids are not helpful; for myasthenia gravis, anticholinesterases and prednisolone may need to be supplemented with intravenous immunoglobulin or plasma exchange; for polymyositis, steroids are the mainstay of treatment. During convalescence patients require understanding and support in coping with residual disability.

Acute Disease↗

Neuropathogenic properties of Argas (Persicargas) walkerae larval homogenates.

Several tick species have been demonstrated, described, or suspected to cause paralysis in their host during the repletion process, presumably by impairing neurotransmission. The resulting polyneuropathy gradually spreads to the upper limbs causing incoordination and ends in respiratory failure. This form of paralysis is commonly confused with Guillain-Barrè syndrome, botulism and myasthenia gravis and although the clinical symptoms of these diseases are similar, it is not clear whether the pathogenesis is also the same. During this study we investigated the mechanism of paralysis by the tick Argas (Persicargas) walkerae by determining the effect of larval homogenates on both potassium-stimulated (calcium-dependent) and veratridine-stimulated (external calcium-independent) release of [3H]glycine from crude rat brain synaptosomes. The results indicated that larval homogenates inhibited both processes. These findings are reconcilable with the results obtained for two other paralysis-causing tick species, Ixodes holocyclus and Dermacentor andersoni, which were indicated to cause paralysis by decreasing the synthesis or release of acetylcholine at the neuromuscular junction.

Animals↗

The localization of a paralysis toxin in granules and nuclei of prefed female Rhipicephalus evertsi evertsi tick salivary gland cells.

A monoclonal antibody directed against a paralysis toxin of Rhipicephalus evertsi evertsi ticks was used to localize the toxin in cytoplasmic granules and, surprisingly, chromatin of the nuclei of cells which resemble the "b" cell type in the salivary glands of Rhipicephalus appendiculatus, Boophilus microplus and Ixodes holocyclus. The association of toxin with chromatin indicates that the toxin may have a regulatory function. Evidence is provided to support the view that the toxin is made up of three identical sub-units, with only the trimeric form being toxic.

Amino Acids↗

Tick toxicosis.

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Ataxia↗

Preliminary survey of ticks (Acari: Ixodidae) parasitizing wild turkeys (Aves: Phasianidae) in eastern Kansas.

During the spring and fall turkey hunting seasons of 1999, hunters and Kansas Department of Wildlife and Parks field personnel examined wild turkeys, Meleagris gallopavo L., for ticks and submitted them to us for identification. From springtime hunting, we received 113 ticks from 12 turkeys killed in nine counties, all in the eastern one-third of Kansas. Collectors reported examining three additional wild turkeys on which no ticks were found. All ticks were nymphal lone star ticks, Amblyomma americanum (L.). Of 11 wild turkeys examined in seven counties during October, one was parasitized by 30 A. americanum larvae. Data from this study and accounts from the published literature suggest that parasitism of wild turkeys by immature lone star ticks is commonplace wherever this host and ectoparasite are sympatric. Our study suggests that M. gallopavo may be an important host that supports lone star tick populations.

Animals↗

Acute flaccid paralysis in Australian children.

OBJECTIVES: To describe the epidemiology and causes of acute flaccid paralysis (AFP) in Australian children, and the clinical features of the two most common causes of AFP, Guillain-Barré syndrome and transverse myelitis. METHODS: Monthly active surveillance for AFP was carried out through the Australian Paediatric Surveillance Unit, with AFP defined as 'acute onset of flaccid paralysis in one or more limbs or of bulbar paralysis in any child less than 15 years of age'. RESULTS: Between March 1995 and December 1999, 143 cases of AFP were reported (approximately 0.8 per 100000 children < 15 years of age per annum). The age range was 2 months-14 years and 59% were boys. Out of these children, 137 (96%) were hospitalized and 47 required intensive care. No case of wild or vaccine-associated poliomyelitis was identified. The most common causes of AFP were Guillain-Barré syndrome in 67 (47%) and transverse myelitis in 27 (19%). Other diagnoses included acute disseminated encephalomyelitis, trauma, tick-bite paralysis and infantile botulism. CONCLUSION: The participation of paediatricians in AFP surveillance contributed to the accreditation of Australia (along with the other 36 countries of the western Pacific region) as 'polio free' by the World Health Organization in October 2000. The surveillance also provided data on the frequency of AFP and identified Guillain-Barré syndrome and transverse myelitis as the most common diagnoses. In this large national series, many other conditions that may present as non-polio AFP were identified.

Acute Disease↗

Diagnostic significance of IgG-synthesizing activated B cells in acute inflammatory diseases of the central nervous system.

An immunohistological technique was used to identify activated, i.e. IgG-synthesizing, B cells in cerebrospinal fluid. A total of 177 patients suffering from inflammatory diseases of the central nervous system were investigated. Activated B cells were found in 61% of patients with bacterial meningitis, especially in lethal or prolonged cases. The number of activated B lymphocytes was low in most cases of viral meningitis, whereas in tick-borne meningopolyneuritis Bannwarth, a very strong B cell activation was detectable. In all inflammatory diseases investigated, the B cell response was restricted to the mononuclear phase. Comparing the number of activated B cells and the amount of locally synthesized IgG, there was a loose correlation between these inflammation parameters in meningopolyneuritis Bannwarth. In acute viral and bacterial meningitis more than 50% of the patients exhibited activated B cells without any detectable intrathecal IgG synthesis.

Antibody Formation↗

Selected neurotoxins.

The small animal practitioner is faced with an infinite number of potential toxins in our modern environment. Unapproved usage of drugs and insecticides requires the practitioner to keep informed about the development of new toxic syndromes. Recreational drug toxicosis in animals is still seen with some frequency in clinical practice and should not be overlooked, even when the owner denies the possible exposure. In this article, we have discussed a few of the more common and newer neurotoxicities seen in clinical practice today. Neurologic toxicities are complex, but treatment can be rewarding if early diagnosis is made and aggressive therapy is instituted. The practitioner will find it worthwhile to establish contact with a toxicologist or poison information center for additional support when necessary.

Animals↗

Pearls and pitfalls in the diagnosis and management of neuromuscular junction disorders.

Myasthenia gravis (MG) is a common autoimmune disorder characterized by the presence of pathogenic antibodies directed against the acetylcholine receptor. Patients present with variable degrees and distribution of fluctuating weakness, at times life-threatening. Clinical manifestations, establishment of diagnosis, the natural history of MG, and therapeutic options are herein reviewed with an emphasis on pearls and pitfalls of clinical relevance. Far less common is Lambert-Eaton syndrome (the myasthenic syndrome), another autoimmune disorder due to the presence of antibodies directed against the PQ-type voltage-gated calcium channels. Clinical features and treatment issues of these and other disorders of neuromuscular transmission are reviewed.

Botulism↗

Neurologic aspects of North American zoonoses.

Neurologic dysfunction is a frequent presentation or complication of zoonotic infections. The differential diagnosis is broad and will include nonzoonotic diseases as well. Patterns of neurologic findings, systemic signs of infection, and epidemiologic risk factors are useful in the approach to diagnosis and initial empiric treatment of the patient with suspected zoonotic infection. Associations between these patterns and specific organisms are emphasized by means of tables and algorithms.

Animals↗