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At least 595 records · Page 33Linked to original sources
PubMed1999

Insulin acts in hypokalemic periodic paralysis by reducing inward rectifier K+ current.

OBJECTIVE: To define how insulin acts in hypokalemic periodic paralysis (HypoPP). BACKGROUND: HypoPP results from point mutations of the skeletal muscle L-type Ca2+ channel. Attacks of flaccid paralysis are associated with hypokalemia and triggered by insulin. A persistent inward current causes depolarization-induced paralysis. The relationships of the Ca2+ channel mutations to the persistent inward current and how insulin triggers paralytic attacks are not yet known. METHODS: Intercostal muscle fibers from HypoPP and normal subjects were studied in vitro at 37 degrees C using two electrodes to determine action potential thresholds and a three-electrode voltage clamp to study membrane currents. RESULTS: HypoPP fibers were depolarized in bathing solution with 4 mM K+. Reducing K+ from 4.0 mM to 2.5 or 1.0 mM depolarized HypoPP fibers but hyperpolarized normal fibers. Adding 12 mU/mL of insulin to bathing fluids increased the depolarization of HypoPP fibers and increased the hyperpolarization of normal fibers. Depolarized HypoPP had increased action potential thresholds. The fraction of excitable muscle fibers decreased with increasing fiber depolarization. Blocking Na+ channels or L-type Ca2+ channels did not prevent depolarization induced by hypokalemia or by insulin. Insulin reduced the conductance of the inward rectifier K+ channel for outward-flowing currents. CONCLUSIONS: Insulin potentiates depolarization of hypokalemic periodic paralysis (HypoPP) fibers by reducing inward rectifier K+ conductance. The Ca2+ mutations in HypoPP indirectly derange membrane excitability by altering the function of other membrane channels.

Adult↗
PubMed2004

A history of Todd and his paralysis.

OBJECTIVE: To describe the history of Robert Bentley Todd (1809-1860) and certain of his contributions to medicine, including his original and subsequent descriptions of "epileptic hemiplegia," which came to be called "Todd's paralysis." METHODS: The author conducted a comprehensive review of English-language literature, modern and historical, related to "Todd's paralysis" and examined Todd's original case histories and commentary by Todd, his contemporaries, and his successors. RESULTS: Todd held that some patients "who recover from a severe fit, or from frequently repeated fits of epilepsy, are often found to labor under hemiplegia, or other modifications of palsy." He believed that this resulted from "undue exaltation. [resulting in] a state of depression or exhaustion." Interestingly, Todd was the first to present an electrical theory of epilepsy, supported by his own animal experimentation, well before his better-known successor John Hughlings Jackson (1835-1911) (famous for his investigations of partial epilepsies and the eponymous "Jacksonian march"). CONCLUSION: Many neurologists and investigators followed Todd in acknowledging transient postictal paralysis as a distinct clinical entity. Yet whether the pathophysiology of "Todd's paralysis" is related to "neuronal exhaustion" or excessive inhibition is still controversial.

History, 19th Century↗
PubMed2005

Temporalis muscle-galea pedicled flap for reconstruction of longstanding facial paralysis.

Reanimation of longstanding facial paralysis is a difficult clinical problem commonly tackled with the method of pedicled muscle flap transfer. The temporalis muscle has been the most popular. In the past, one common problem was that the flap was not long enough to reach parts of the face distant from the affected area. To overcome this disadvantage, we have devised a flap consisting of the pedicled temporalis muscle, temporal fascia and galea together and have achieved good static results in paralyzed faces. From June, 1996 to May, 2003, we used this procedure with 38 longstanding facial paralysis patients (16 male and 22 female); 23 had right-sided and 15 had left-sided facial paralysis. The patients were followed-up over three years. Our results were recorded as "Excellent", "Good", "Fair" or "Poor". Excellent or good results were obtained in 33 patients (87%). In these patients, the static results are very good. The oral commissure on the affected side maintained a favorable position and almost complete symmetry of expression was attained. We have achieved dynamic reconstruction by using a temporalis muscle-galea pedicled flap in 38 longstanding facial paralysis patients. Our results show that this is a good option in treating such patients.

Adult↗
PubMed1986

Cheiloplasty in the treatment of facial paralysis.

There have been dramatic improvements in the treatment of facial paralysis. These include the successful use of free autogenous nerve grafting, nerve crossover techniques, regional masticatory muscle transposition, and free muscle grafts. The techniques are applied to total, partial, and regional paresis. The bulk of information on rehabilitation of the face has come from clinical empiricism, but basic research in nerve and muscle physiology and attempts at multiple classifications regarding indications and criteria have added to the splendor of this drama. One facet that has not been emphasized is the use of cheiloplasty in long-standing facial paralysis. Long-standing facial paralysis has both a neural and muscular deficit that cannot be rectified by a single concept or operation. It is essential to regionalize the rehabilitation, implant a kinetic muscular potential, supply some static support and elevation, and address the nonfunctional muscles about the paralyzed lips. This latter concept includes lip shortening and lip-flap transposition. A coordinated combination of these techniques has the best opportunity of maximizing the improvement in long-standing facial paralysis associated with severe muscle atrophy.

Chronic Disease↗
PubMed1990

Vocal cord paralysis in children.

Bilateral vocal cord paralysis is a common cause of stridor in infants and children. There are significant differences in this entity between children and adults with regard to etiology, diagnosis, management, and outcome. A review of 10 years' experience at Children's Hospital of Philadelphia identified 51 children seen with the diagnosis of vocal cord paralysis. These cases were evaluated with respect to etiology of paralysis, whether unilateral or bilateral, delay in diagnosis, need for tracheotomy, abnormality of voice, surgical treatment, and outcome. Guidelines for management for a child with vocal cord paralysis are presented with emphasis on flexible endoscopic evaluation and conservative management.

Child↗
PubMed1993

Configuration of the glottis in laryngeal paralysis. I: Clinical study.

It is widely accepted in the American literature that the cricothyroid muscle is responsible for the paramedian position of the vocal fold in recurrent laryngeal nerve paralysis. However, support in the literature for this theory is not conclusive, and the cadaveric vocal fold position expected after lesions of the vagus nerve has also been reported in patients with an intact superior laryngeal nerve. This study compares the configuration of the glottis in patients with unilateral paralysis due to known lesions of either the recurrent laryngeal or vagus nerve. Normal subjects were studied as controls. Results indicate that the alteration of glottic configuration in laryngeal paralysis cannot be adequately characterized by standard terms of vocal fold position. The paralyzed vocal fold is shortened, with anterior rotation of the arytenoid. Patients with vagus nerve lesions had a statistically insignificant tendency for a more lateral vocal fold position, but a discrete difference in position between the two groups was not identified. This study also confirms prior observations that paralyzed vocal folds are frequently not denervated. These findings have significant implications for management of laryngeal paralysis.

Adult↗
PubMed1993

Configuration of the glottis in laryngeal paralysis. II: Animal experiments.

It is widely believed that in isolated recurrent laryngeal nerve paralysis, the paralyzed vocal fold assumes a median or paramedian position, due to the action of the cricothyroid muscle. A review of the literature reveals that support for this theory is not conclusive and, in particular, experiments indicate that the cricothyroid muscle does not appreciably affect vocal fold position in acute paralysis. The research in this study compares the configuration of the glottis in chronic unilateral recurrent laryngeal nerve paralysis in cats, with and without concomitant denervation of the cricothyroid muscle. Results indicate that vocal fold position is not determined by the cricothyroid muscle. Incomplete denervation of intrinsic laryngeal muscles as well as synkinetic reinnervation appear to be significant factors in determining vocal fold position in chronic laryngeal paralysis.

Animals↗
PubMed1995

The cricothyroid muscle does not influence vocal fold position in laryngeal paralysis.

The status of the cricothyroid muscle, which is innervated by the superior laryngeal nerve, is believed to influence the vocal fold position in laryngeal paralysis. It is believed that isolated lesions of the recurrent laryngeal nerve generally result in the paralyzed vocal fold assuming a paramedian position but that with lesions of both the superior and recurrent laryngeal nerves, a more lateral (intermediate or cadaveric) vocal fold position can be expected. Twenty-six consecutive patients with unilateral vocal fold paralysis underwent transnasal fiberoptic laryngoscopy (TFL) and laryngeal electromyography (LEMG). By TFL, the vocal fold positions were paramedian in 8 patients, intermediate in 7, and lateral in 11. By LEMG, 13 patients had isolated recurrent laryngeal nerve lesions and 13 patients had combined (superior and recurrent laryngeal nerve) lesions. There was no correlation between the vocal fold position and the status of the cricothyroid muscle, i.e., the status of the cricothyroid muscle by LEMG did not predict the vocal fold position nor did the vocal fold position by TFL predict the site of lesion. In addition, we investigated the possibility that the degree of thyroarytenoid muscle recruitment (tone) might correlate with vocal fold position, but no relation was found. We conclude that 1. the cricothyroid muscle does not predictably influence the position of the vocal fold in unilateral paralysis; 2. thyroarytenoid muscle recruitment (tone) does not appear to influence vocal fold position; and 3. still unidentified and unknown factors may be responsible for determining vocal fold position in laryngeal paralysis.

Adolescent↗
PubMed2005

Sound signature for identification of tracheal collapse and laryngeal paralysis in dogs.

The aims of this study were to investigate whether upper airway sounds of dogs with laryngeal paralysis and tracheal collapse have distinct sound characteristics, compared with unaffected dogs. The sounds of 5 dogs with laryngeal paralysis and 5 dogs with tracheal collapse were recorded. Honking sound appeared as predominant clinical signs in dogs with tracheal collapse. Laryngeal stridors appeared as predominant clinical signs in dogs with experimentally produced laryngeal paralysis by resection of laryngeal nerve, in which two types of stridor, I and II, were recorded. All these sounds were analyzed using sound spectrogam analysis. There were significant differences in duration (sec), intensity (dB), pitch (Hz), first formant (Hz), second formant (Hz), third formant (Hz), fourth formant (Hz) of sounds between the normal bark and two types of stridor or honking sound, indicating that the sound analysis might be a useful diagnostic modality for dogs with tracheal collapse and laryngeal paralysis.

Animals↗
PubMed2005

Thyrotoxic hypokalemic periodic paralysis in a Turkish male with graves' disease: a rare case report and review of the literature.

Thyrotoxic hypokalemic periodic paralysis (THPP) is a very rare complication of thyrotoxicosis in whites, but is more frequently reported in individuals of Asian descent. Hypokalemia, with associated flaccid paralysis, and signs of hyperthyroidism, are the hallmark. We have reported a case of a 28-yr-old white man with Graves' disease presenting with a 2-wk history of episodic flaccid quadriplegia. Physical examination disclosed a resting tachycardia and symmetrical, proximal weakness involving both arms and legs. Electrocardiogram and electrolyte analysis showed a severe hypokalemia, and thyroid function tests revealed hyperthyroidism. The patient was diagnosed as having Graves' hyperthyroidism and THPP. Paralysis resolved with potassium supplements. He was treated with propranolol and, subsequently, methimazole. He had no further episodes of hypokalemic paralysis. To the best of the author's knowledge, and after a Medline search, THPP has not been described previously in a Turkish man.

Adult↗
PubMed2005

Thyrotoxic periodic paralysis in a Turkish male; the recurrence of the attack after radioiodine treatment.

Thyrotoxic hypokalemic periodic paralysis (THPP) is a rare complication of hyperthyroidism and an uncommon form of hypokalemic periodic paralysis. Its differentiation of more common forms of periodic paralysis is important because aggressive treatment can place the patient at risk for rebound hyperkalemia. Treatment of the underlying thyroid dysfunction cures the muscle symptoms. Here we describe a 37-year-old Turkish male with THPP whose paralysis attack recurred soon after administration of radioactive iodine.

Adrenergic beta-Antagonists↗
PubMed2004

[Thyrotoxic hypokalemic periodic paralysis, an endocrine emergency: clinical and genetic features in 25 patients].

Thyrotoxic hypokalemic periodic paralysis (THPP) is a medical emergency characterized by acute attacks of weakness, hypokalemia, and thyrotoxicosis that resolve with the treatment of hyperthyroidism. Attacks are transient, self-limited, associated with hypokalemia and resemble those of familial hypokalemic periodic paralysis (FHPP), an autosomal dominant neurological channelopathy. This study reviews the clinical features and genetic findings of THPP in 25 Brazilian patients. Most patients had weight loss, taquicardia, goiter, tremor, and ophthalmopathy. Most often attacks arose during the night and recovered spontaneously but some patients evolved to total quadriplegia, and few experienced cardiac arrhythmias. All patients had suppressed TSH and elevated T4 and most had positive anti-thyroid antibodies, indicating autoimmunity thyrotoxic etiology. Potassium was low in all patients during the crisis. Prophylactic potassium therapy has not been shown to prevent attacks; however it was useful for curbing the paralysis during the crisis. We identified the mutation R83H in the KCNE3 gene in one sporadic case, and M58V in the KCNE4 gene in one case with family history. Furthermore, we identified other genetic polymorphisms in the CACNA1S, SCN4A, KCNE1, KCNE2, KCNE1L, KCNJ2, KCNJ8 e KCNJ11 genes. We conclude that THPP is the most common treatable cause of acquired periodic paralysis; therefore, it must be included in the differential diagnosis of acute muscle weakness.

Adolescent↗
PubMedDate not supplied

[Mime functional evaluation in facial paralysis following a stroke].

BACKGROUND: Functional evaluation of the facial movements in patients with facial paralysis following a stroke. AIM: To evaluate the function of the facial muscles of patients after central facial paralysis following a stroke. METHOD: Nine patients referred by the Neurology Service were evaluated. The evaluation focused on spontaneous, voluntary and reflex movements. RESULTS: Reflex and voluntary movement of the eyelid and forehead were preserved in all patients. However, spontaneous and voluntary movements of the lips and nose were limited according to the location and extension of lesion. CONCLUSION: The symptoms of central facial paralysis, in which paralysis only of voluntary movements of the lower two-thirds of the face is expected, occurred in the minority of the patients.

Adult↗
PubMedDate not supplied

Thyrotoxic periodic paralysis complicated with primary aldosteronism.

A 35-year-old man presented with acute onset of bilateral lower extremity weakness after ingesting a large amount of carbohydrates. Laboratory investigation revealed severe hypokalemia (1.9 mEq/l) and hyperthyroidism. The patient also exhibited primary aldosteronism due to a left adrenal adenoma. As a diagnostic tool, paralysis with hypokalemia (2.8 mEq/l) was induced with a glucose infusion. After treatment with methimazole, there were no further episodes of paralysis and subsequent induction of paralysis with glucose was impossible, though primary aldosteronism persisted. These findings indicate that hyperthyroidism played a major role in the development of periodic paralysis, while primary aldosteronism apparently increased the patient's vulnerability to paralytic attacks.

Adenoma↗
PubMed1988

The significance of stapedial reflex test in facial nerve paralysis.

The stapedial reflex of 30 patients with peripheral facial nerve paralysis was compared with the results of facial paralysis scores. The stapedial reflex was measured with an oto-reflex analyser, RS-06A. The stimulation frequencies in the stapedial reflex test were 500, 1,000 and 2,000 Hz for both ipsilateral and contralateral stimulation. The stapedial reflex test at 500 Hz for contralateral stimulation seemed to be useful for evaluating the degree of facial paralysis. With 500 Hz or 1,000 Hz contralateral stimulation, the stapedial reflex test seemed to be useful for predicting the prognosis for facial nerve paralysis. In these stimulations, cases with a positive reflex within 2 weeks showed complete recovery within 12 weeks, and cases with positive reflex within 4 weeks showed recovery within 24 weeks.

Adolescent↗
PubMed1988

Prognostic value of blink test in patients with facial paralysis.

In order to gain an early estimate of a prognosis for facial paralysis, the vertical eye movements associated with eyeblinks (Bell's phenomenon) in 39 patients with acute unilateral Bell's paralysis and Hunt's syndrome and of 21 normal subjects were recorded by electronystagmography. These data were then analysed with a small digital computer (PDP 11/34). The results were compared with electroneurography (ENoG) and nerve excitability test (NET) results and can be summarized as follows: 1. Difference in velocity and amplitude between left and right eye movement during eyeblink (called blink index), diminished in inverse proportion to any improvement of lagophthalmos. 2. All the 5 patients showing more than 80% in maximum blink index (MBI) proved to have a poor prognosis, whereas 18 of 19 patients having a MBI of 40% or less proved to have a good prognosis. The blink test was deemed to be of equal clinical significance to ENoG and NET for predicting facial paralysis. 3. The blink test does not require needle electrodes for electrical stimulus, nor any special equipment other than electronystagmography, and yet this test can provide a quantitative analysis of a degeneration profile in facial paralysis.

Blinking↗
PubMed1988

Pathological features of peripheral facial paralysis caused by malignant tumour.

It has been reported that tumour invasion of the facial canal does not necessarily produce facial paralysis. The purpose of this paper is to present the facial nerve pathology in cases of facial paralysis caused by malignant neoplasms. Forty-seven temporal bones acquired from patients who died of malignant neoplasms were used for this analysis. Of the 47, 18 temporal bones (38.3%) had temporal bone metastasis or invasion. In 6 cases, the tumour destroyed the bony facial canals exposing the facial nerves to the invading tumour cells. The records of the patients showed that only half of the patients had facial paralysis. Those in whom tumour cells invaded the facial nerve beyond the epineural sheath had complete facial paralysis before death.

Bone Neoplasms↗
PubMed1991

Decussation of hind-limb and fore-limb fibers in the monkey corticospinal tract: relevance to cruciate paralysis.

Cruciate paralysis is a clinical entity in which patients with trauma to the anterior cervicomedullary junction present with weakness of the upper extremity greater than that of the lower extremity. The underlying mechanism of this paralysis is commonly thought to be selective damage affecting the upper-extremity nerve fibers in the pyramidal decussation. The authors examined the anatomical basis of cruciate paralysis in six New World squirrel monkeys and two Old World cynomolgus monkeys. No evidence for a differential decussation of fore-limb and hind-limb fibers was found. Thus, there is no obvious anatomical explanation for cruciate palsy. The results do suggest two alternative explanations for cruciate paralysis: 1) selective damage to neural areas involving the internuncial cells, the central gray area, and the cuneate nucleus, or 2) injury to the ventral corticospinal tract.

Animals↗