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At least 37 records · Page 2Linked to original sources
PubMed1995

Facial nerve paralysis induced by herpes simplex virus in mice: an animal model of acute and transient facial paralysis.

We have been the first to succeed in producing an acute and transient facial paralysis simulating Bell's palsy, by inoculating herpes simplex virus into the auricles or tongues of mice. The KOS strain of the virus was injected into the auricle of 104 mice and the anterior two thirds of the tongue in 30 mice. Facial paralysis developed between 6 and 9 days after virus inoculation, continued for 3 to 7 days, and then recovered spontaneously. The animals were painlessly sacrificed between 6 and 20 days after inoculation for histopathologic and immunocytochemical study. Histopathologically, severe nerve swelling, inflammatory cell infiltration, and vacuolar degeneration were manifested in the affected facial nerve and nuclei. Herpes simplex virus antigens were also detected in the facial nerve, geniculate ganglion, and facial nerve nucleus. The pathophysiologic mechanisms of the facial paralysis are discussed in light of the histopathologic findings, in association with the causation of Bell's palsy.

Animals↗
PubMed1986

Bilateral upper extremity paralysis (Bell's cruciate paralysis) from a gunshot wound to the cervicomedullary junction.

Cruciate paralysis is characterized by midline involvement of the rostral portion of the pyramidal decussation, resulting in paralysis of the upper extremity without lower extremity involvement. The neuroanatomical basis is the more rostral and medial decussation of the upper extremity motor fibers in the medulla compared with the more caudal and lateral decussating fibers of the lower extremity at the lower boundary of the cervicomedullary junction. We believe this to be the first reported case of Bell's cruciate paralysis caused by a gunshot wound to this region. The neuroanatomical basis and the mechanisms that produce this unique clinical entity are discussed.

Arm↗
PubMed2001

Propranolol rapidly reverses paralysis, hypokalemia, and hypophosphatemia in thyrotoxic periodic paralysis.

Hypokalemia and hypophosphatemia are commonly encountered during paralysis in patients with thyrotoxic periodic paralysis (TPP) and may contribute to neuromuscular manifestations. Potassium and phosphate supplements have been recommended to hasten recovery and prevent cardiopulmonary complications. However, this recommendation has not yet proven efficacious. Hyperadrenergic activity has been implicated in the pathogenesis of TPP. We tested whether nonselective beta-blockers could terminate neuromuscular symptoms rapidly while reducing an intracellular shift of potassium and phosphate. We describe two patients who had an acute attack of TPP with characteristic hypokalemia and hypophosphatemia associated with low urinary potassium and phosphate excretion. After oral propranolol, 3 mg/kg, serum potassium and phosphate concentrations increased promptly in 2 hours in both patients, and there was complete amelioration of paralysis. No rebound hyperkalemia or hyperphosphatemia was detected. Given their efficacy in this pilot study, they should be considered as a first-line therapy for TPP.

Administration, Oral↗
PubMed1976

A new standardized and effective method of inducing paralysis without administration of exogenous hormone in patients with familial periodic paralysis.

A prolonged glucose loading test is described. When used in five patients with familial periodic paralysis it brought them into a state of massive hypopotassaemic paralysis at the first attempt, without the use of exogenous hormone. Three normal persons were subjected to the same glucose loading without exhibiting hypopotassaemia or muscular weakness. There were no essential differences in serum glucose levels between the two groups of individuals. The efficacy of previous methods of inducing paralysis, hormonal as well as non-hormonal, is reviewed, and the advantages of this new method are pointed out.

Blood Glucose↗
PubMed2005

Detection of chronic bee paralysis virus and acute bee paralysis virus in Uruguayan honeybees.

Chronic bee paralysis virus (CBPV) causes a disease characterized by trembling, flightless, and crawling bees, while Acute bee paralysis virus (ABPV) is commonly detected in apparently healthy colonies, usually associated to Varroa destructor. Both viruses had been detected in most regions of the world, except in South America. In this work, we detected CBPV and ABPV in samples of Uruguayan honeybees by RT-PCR. The detection of both viruses in different provinces and the fact that most of the analyzed samples were infected, suggest that, they are widely spread in the region. This is the first record of the presence of CBPV and ABPV in Uruguay and South America.

Acute Disease↗
PubMed1997

Thyrotoxic periodic paralysis; a reversible cause of paralysis to remember.

A young Chinese American male presented with progressive proximal muscle weakness and inability to stand and walk. Investigations revealed marked hypokalemia and thyroid studies revealed hyperthyroidism consistent with Graves' disease. Thyrotoxic periodic paralysis is a rare disorder in the Western hemisphere, yet needs to be considered as a cause particularly in patients of Oriental origin presenting with sudden weakness. The case history and update of current knowledge of thyrotoxic periodic paralysis is presented.

Adult↗
PubMed1999

[Medication-induced vocal cord paralysis as an uncommon cause of cord paralysis].

A case is reported of a 57-year-old man who was found to have a right vocal cord paralysis that most likely followed prolonged treatment with the anti-arrythmic medication Amiodaron-HCl (Cordarex). Phoniatric treatment was given for 5 1/2 months, during which time microlaryngoscopy and stroboscopy were performed. With the help of speech therapy, mobility of the paralyzed cord was seen to begin to return 3 1/2 months after discontinuing the Amiodaron-HCl. Full cord mobility has not returned to date.

Amiodarone↗
PubMed1999

Surveillance of acute flaccid paralysis in Italy: 1996-1997. AFP Study Group. Acute flaccid paralysis.

The last case of poliomyelitis due to transmission of indigenous wild poliovirus occurred in Italy in 1982. To achieve the certification of the eradication of poliomyelitis in Italy, an active surveillance of acute flaccid paralysis (AFP) in the population aged less than 15 years was set up following the World Health Organization (WHO) guidelines. The survey started in 1996 with a pilot study involving 4 out of 21 regions, and was gradually extended to a national level in 1997. The two-year survey identified five patients with diagnosis of vaccine associated paralytic poliomyelitis (VAPP). Polioviruses type 2 and 3 Sabin-like were isolated and characterized in three of them. In the remaining two cases, samples were collected late after the onset of symptoms, and poliovirus could not be isolated. No wild polioviruses were detected during the survey. The rate of non-polio AFP found in Italy in 1997 was 0.61 cases per 100,000, which is lower than the level of 1.0 case per 100,000 considered as acceptable by the WHO. This was mainly due to the delay in organizing the hospital network and starting the active search of AFP cases in the largest and most densely populated regions. Therefore, the overall rate of AFP found in Italy underestimates the global effectiveness of the program, which however will be better evaluated in the next few years. This study is the first systematic attempt to determine the rate of AFP in Italy.

Adolescent↗
PubMed1990

Diaphragmatic paralysis without bulbar or limb paralysis in multiple sclerosis.

A patient is presented in whom disabling pulmonary symptoms in the absence of other significant disability complicated a long-standing course of MS. Clinical presentation and fluoroscopy confirmed the diagnosis of bilateral diaphragmatic paralysis. Magnetic resonance imaging revealed atrophy and extensive white matter changes within the cervical cord. This case is unique in that significant respiratory compromise due to cervical spinal cord involvement by MS was dissociated from bulbar dysfunction or profound limb paresis.

Adult↗