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PubMed1981

Induction of spinal cord paralysis by negative pi-mesons.

As part of our investigations on late non-neoplastic injury induced by negative pi-mesons (pions), a series of studies have been performed using pion beams for the induction of spinal cord paralysis in the Fisher 344 rat. Groups of rats were exposed to 1, 5 or 15 daily doses of peak pions or X rays. Paralysis appeared earlier after treatment with pions than after X rays even in a comparison of groups with similar final incidences. A single dose RBE for spinal cord paralysis of 1.3 was found. The RBE rises to a value of 3.2 if the total dose is given as a series of 15 daily exposures. These RBEs are far larger than we have observed using other late injury end-points, such as tubular degeneration in the kidney or fibrosis and sclerosis in the support structures of the colon for which the single dose RBE is less than 1.2. The biological and/or physical basis for the high sensitivity of the spinal cord to peak pions has not yet been resolved, but these data have suggested caution in exposing the spinal cord to peak pions in our clinical trials.

Animals↗
PubMed2002

Case report: bilateral vocal cord paralysis caused by cervical spinal osteophytes.

Thyroid and cervical surgery, tracheal intubation, trauma and neurodegenerative and neuromuscular diseases may cause bilateral vocal cord paralysis. There are only a few reported cases of bilateral cord paralysis associated with cervical hyperostosis in the English literature. We report the MR and CT findings of a case of bilateral vocal cord paralysis caused by cervical spinal osteophytes compressing the recurrent laryngeal nerves.

Aged↗
PubMed1978

Gelfoam paste injection for vocal cord paralysis: temporary rehabilitation of glottic incompetence.

Vocal cord paralysis frequently results in open glottic incompetence with aspiration, an ineffective cough, and poor voice production. Glottic competence can be restored temporarily be injecting the true vocal cord with Gelfoam paste. This clinical use of Gelfoam for temporary rehabilitation is indicated in : 1) situations in which paralysis may be temporary, 2) patients for whom an open operative procedure must be delayed, and 3) circumstances in which it is desirable to determine the effect of vocal cord injection prior to placement of nonabsorbable material. The injection of Gelfoam paste results in minimal tissue reaction. Absorption is gradual over a period of six to ten weeks, allowing time for some glottic compensation. The injection may be repeated without adverse effects until the paralysis resolves or intervention of a permanent nature is indicated.

Gelatin Sponge, Absorbable↗
PubMed1979

The opercular syndrome--diagnostic trap in facial paralysis.

We describe a patient with a left facial paralysis and hemotympanum following left parieto-occipital skull trauma. The initial admission diagnosis of intratemporal facial nerve injury secondary to temporal bone fracture was incorrect. Normal facial movements during involuntary activity (yawning, laughing at a joke) and focal seizure activity on the paralyzed side of the face, seen subsequently, indicated the site of lesion as supranuclear. The diagnosis of opercular syndrome was made. This syndrome can result when the contralateral frontal lobe is injured. Supranuclear weakness of muscles supplied by the hypoglossal or spinal accessory nerves is also present. Unlike other central paralyses, the facial paralysis in operculum syndrome may not demonstrate "forehead sparing" and consequently it may be mistaken for a peripheral paralysis. The neuroanatomic basis for the syndrome is discussed. Signs and symptoms are outlined to help the otolaryngologist avoid this diagnostic pitfall.

Adult↗
PubMed1982

Transient vocal paralysis following strangulation injury.

Blunt trauma to the larynx, as a source of vocal paralysis, has become an important consideration for the laryngologist. Direct neurologic injury from strangulation by hand is explored with presentation of 4 patients. Three of these had unilateral paralysis; the fourth had bilateral paralysis on two separate occasions of strangulation. All patients recovered in 4 to 20 days. Correlation is made with other acute nerve compression syndromes, and the pathophysiology discussed in light of experimental evidence. Awareness and recognition of this problem in evaluation and treatment of strangulation assault injuries is stressed.

Adolescent↗
PubMed1989

Facial reanimation by XI-VII anastomosis without shoulder paralysis.

Transposition of the spinal accessory (XI) and facial (VII) nerves has been used successfully in reanimation of facial paralysis, but because of the severity of symptoms associated with denervation of the trapezius muscle, this technique has largely been abandoned. Hypoglossal-facial (XII-VII) nerve anastomosis has now become a more favored procedure; however, the resultant hemiglossal atrophy carries some morbidity. Transposition of the sternocleidomastoid (SCM) branch of the accessory nerve as a way to avoid shoulder paralysis was reported more than 20 years ago with initially excellent results, yet few follow-up studies have been done. Twenty-one fresh cadaver dissections of the accessory nerve-SCM branch and facial nerve were performed to determine if adequate numbers of fascicle groups and sufficient proximal nerve length are available for an adequate end-to-end anastomosis without nerve interposition grafting. This paper presents our anatomic and histologic findings to support the use of proximal SCM nerve anastomosis to distal facial nerve in facial reanimation. When feasible, the use of this technique to correct facial paralysis is encouraged rather than hypoglossal-to-facial nerve anastomotic repair.

Accessory Nerve↗
PubMed1983

Post-traumatic facial nerve paralysis: three cases of delayed temporal bone exploration with recovery.

No consensus exists today on the management of immediate-onset post-traumatic facial nerve paralysis. Controversy surrounds the timing of surgical intervention and the role of electrophysiologic testing. Three patients are presented who sustained immediate, complete facial paralysis following closed head trauma. They did not have prompt facial nerve decompression. In each case, electroneurography and electromyography showed complete nerve degeneration and denervated muscle. Despite the results of the electrophysiologic tests, all patients underwent late surgical decompression of the nerve: one at 2 1/2 months, one at 3 months, and one as late as 14 months after injury. They all had good recovery of facial function within 6 months of surgery. Early surgical intervention has been advocated in post-traumatic facial nerve paralysis if any benefit is to be gained. It is thought that late surgical intervention is unlikely to yield further improvement in the facial nerve function. Experience with these cases suggests that surgical exploration of the facial nerve is indicated at anytime, as it may be beneficial even in very old injuries. The prognostic value of electroneurography and electromyography in determining facial nerve recovery and in deciding upon facial nerve surgery is questioned.

Adult↗
PubMed1984

Endoscopic laser arytenoidectomy for the treatment of bilateral vocal cord paralysis.

Most patients with bilateral vocal cord paralysis have a fairly satisfactory voice, but their airway is usually compromised. The management of such patients presents a challenge to the otolaryngologist-head and neck surgeon. Numerous surgical procedures have been developed in an attempt to improve the patients's airway insufficiency without leaving him with a breathy, weak voice. Arytenoidectomy is currently the most reliable method of treating patients with bilateral vocal cord paralysis. Although both endoscopic and external approaches have been described for performing an arytenoidectomy, the endoscopic technique is more desirable since it requires no incision and theoretically allows for the immediate assessment of airway size. The addition of the CO2 laser to the surgical armamentarium offers certain refinements to the technique of endoscopic arytenoidectomy. Eleven patients with bilateral vocal cord paralysis of the larynx have been treated by endoscopic laser arytenoidectomy by the authors utilizing a technique developed by the two senior authors and subsequently taught to over 200 participants of the CO2 laser workshops sponsored by the Department of Otolaryngology-Head and Neck Surgery at Northwestern University Medical School; 10 of the 11 patients have been successfully decannulated. The technique and problems of this operation will be discussed.

Aged↗
PubMed1985

Vocal cord paralysis and recovery with thyroid lymphoma.

Vocal cord paralysis has been reported in 33 patients with thyroid lymphoma for an estimated overall incidence of 17%. There is little expectation of vocal cord function recovery, both because neoplastic invasion is believed irreversible and since surgery often necessitates sacrifice of the recurrent laryngeal nerve. Unlike in most well differentiated thyroid malignancies, external radiation therapy plays a vital role in the treatment of thyroid lymphoma. The patient presented here had complete recovery of vocal cord function following radiation therapy for a large thyroid lymphoma associated with vocal cord paralysis. This is the first reported case of such recovery following treatment for a thyroid neoplasm. The rather rapid and complete recovery of neural function suggests that, at least in some, paralysis is caused by reversible compression rather than by neural invasion or tumor-induced neurolysis.

Aged↗
PubMed2006

Drug-induced thyrotoxic periodic paralysis.

OBJECTIVE: To report a case of iodine-induced (Jod-Basedow) hyperthyroidism leading to thyrotoxic periodic paralysis (TPP). CASE SUMMARY: A 64-year-old white male, one day status-post-cardiac catheterization, presented to the local emergency department with profound weakness of his extremities and an inability to stand on his own. Pertinent laboratory test results included a potassium level of 3.0 mEq/L. Treatments of oral and intravenous potassium supplementation resulted in his complete recovery. Two days later he was diagnosed with hyperthyroidism and subsequently treated with nadolol 40 mg daily and methimazole 20 mg daily. At time of writing, the patient remained euthyroid, receiving no antithyroid medications. There had been no further reports of paralysis in the 6 years since his original presentation. The Naranjo probability scale indicated a probable relationship between the patient's episode of TPP and his exposure to the iodinated contrast dye. DISCUSSION: TPP is an uncommon manifestation in white patients with hyperthyroidism. Iodine-induced TPP is even more rare, with only 2 such cases reported as of November 2, 2005. In this case, Jod-Basedow hyperthyroidism was induced by the iodine-containing dye that the patient received during cardiac catheterization. Soon after the dye was administered, he developed TPP. CONCLUSIONS: Clinicians should be aware not only of potential causes of drug-induced thyroid disease, but also of the potential for drug-induced hyperthyroidism leading to TPP. The diagnosis of TPP should be considered in patients presenting with acute onset of extremity weakness or paralysis and hypokalemia. Quick diagnosis and prompt treatment of TPP can prevent life-threatening complications of this treatable and curable disorder.

Contrast Media↗
PubMed2000

Bilateral diaphragm paralysis secondary to central von Recklinghausen's disease.

Bilateral paralysis of the diaphragm is either idiopathic or associated with several medical conditions, including trauma or thoracic surgery, viral infections, and neurologic congenital or degenerative disorders. We describe the case of a 36-year-old man with a history of neurofibromatosis who developed severe bilateral diaphragmatic paralysis from involvement of the phrenic nerve roots with neurofibromas. The patient manifested progressive exertional dyspnea and debilitating orthopnea requiring the use of noninvasive mechanical ventilation at night. A review of the literature reveals that neurofibromatosis is an unrecognized cause of diaphragmatic paralysis.

Adult↗
PubMed1983

Temporary muscle paralysis for accurate measurement of pulmonary artery occlusion pressure.

Succinylcholine, a short-acting neuromuscular blocking agent, was used to accurately measure the pulmonary artery occlusion pressure (PAOP) in eight patients requiring mechanical ventilation for acute respiratory failure, in whom measurement was difficult because of significant respiratory variation in PAOP. The mean decrease in PAOP after paralysis was 9.8 +/- 5.3 mm Hg, with a range of 4 to 20 mm Hg (p less than 0.01). The magnitude of change was closely correlated to the degree of respiratory variation in PAOP observed during spontaneous breathing before paralysis (r = 0.889). Accurate measurement of PAOP affected subsequent management in five of these eight patients. Temporary muscle paralysis with succinylcholine is a useful means of eliminating artifactual elevations in PAOP in patients supported by mechanical ventilation when significant respiratory variation in PAOP is present.

Adult↗
PubMed1994

[A case of Shy-Drager syndrome complicated with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and incomplete paralysis of bilateral vocal cords].

A 67-year-old man with SIADH complicated by slowly progressing autonomic failure was described. The patient noticed constipation at the age of 57. In the following years, he suffered from urinary incontinence, depletion of sweating, impotence, sleeplessness with snore, and dizziness while walking. Physical examination revealed a masked oily face with slight cerebellar disturbance. Abnormality of autonomic function tests was recognized and he was diagnosed as Shy-Drager syndrome with gradually progressing, diffuse autonomic failure accompanied by slight cerebellar ataxia and Parkinsonism. Both serum sodium level and plasma osmotic pressure were reduced, whereas daily sodium excretion was more than 100mEq and urinary osmolality was about 500mOsm/kgH2O. His renal function was intact, and the adrenocortical and thyroid hormone levels were normal, then criteria of SIADH was fulfilled. SIADH was thought to have occurred on the basis of Shy-Drager syndrome. Water load test showed failure of adequate water diuresis, but intravenous phenytoin administration following the water load test ameliorated the diuresis to normal. The relationship between plasma osmolality and the ADH response indicates that ADH was adequately secreted in response to the increase in plasma osmolality but not suppressed in response to the decrease in plasma osmolality below 280mOsm/kgH2O. These results suggest that ADH synthesis in the hypothalamus and its secretion from the pituitary gland were both intact. The response of ADH secretion to the orthostatic hypotension induced by head-up tilt was quite blunted, being compatible with Shy-Drager Syndrome. Sleep disturbance was studied by polysomnography and laryngoscopy, and was revealed to be based upon severe sleep apnea due to incomplete paralysis of the bilateral vocal cords. Sleep apnea due to vocal cord paralysis is sometimes found to be complicated in patients with multiple system atrophy (MSA) including Shy-Drager syndrome, and is known as Gerhardt syndrome. This is the first report on a case of Shy-Drager syndrome complicated with SIADH and bilateral vocal cord paralysis. In this case, SIADH is caused by impaired afferent pathways from baroreceptors to the hypothalamus, which transfer inhibitory stimuli on ADH secretion. It is suggested that Shy-Drager syndrome should be considered one of the causes of SIADH.

Aged↗
PubMed1976

Changes in plasma renin activity and plasma aldosterone in the induced paralytic attack of thyrotroxic periodic paralysis.

Changes in serum electrolytes, haematocrit, plasma renin activity and plasma aldosterone induced by glucose and insulin (GI) infusion were serially investigated in seven patients with periodic thyrotoxic paralysis. An attack which developed into complete quadriplegia was induced within 90 min after the beginning of the GI infusion in four out of seven patients. Only a slight paralysis of the legs was produced in another two patients and induction of an attack did not materialize in one. In four patients with complete quadriplegia, the mean values of serum sodium and potassium concentrations, haematocrit, plasma renin activity and plasma aldosterone slightly decreased immediately after the beginning of the GI infusion. Induction of a paralytic attack was not accompanied by any significant changes in serum sodium concentration, haematocrit, plasma renin activity and plasma aldosterone either 15 min before or after the onset of attack, while the serum potassium concentration progressively decreased, and an increase in plasma aldosterone associated with an increase of haematocrit and plasma renin activity reached a peak level at the stage of complete quadriplegia. On the other hand, in the three patients in whom an infusion produced slight or no paralysis of the legs, changes in the serum sodium concentration, haematocrit, plasma renin activity and plasma aldosterone were insignificant and the serum potassium concentration was slightly but insignificantly decreased. These results suggest that hyperaldosteronism may not be a trigger for the induced paralytic attack but a phenomenon secondary to volume depletion and a change in potassium homoeostasis induced by GI infusion.

Adult↗
PubMed2005

[Thyrotoxic hypocalemic periodic paralysis: report of 3 cases].

Thyrotoxic hypokalemic periodic paralysis (THPP) is a rare hyperthyroidism complication much more frequent in Asians and Caucasians. We present 3 cases of THPP occurring in Brazilian male patients with 28 years old (y) (Case 1), 29 y (Case 2) and 60 y (Case 3), respectively. They were admitted following an episode of flacid paralysis of extremities. Whereas case 1 reported recurring episodes of paralysis crises, cases 2 and 3 reported only one episode. Signs and symptoms of thyrotoxicosis, such as weigh loss, diaphoresis, extremities tremor, palpitation and mild diffuse goiter were present in the first case; while the second case only presented ophthalmopathy and the third patient referred that 2 years before his admission he presented an episode of cardiac arrhythmia but did not have thyroid function evaluation at that time. Their laboratory findings were hypokalemia, low TSH and raised free T4. They were treated with intravenous potassium, oral propranolol and tiamazol with remission of the symptoms. We report these cases to emphasize the importance of recognizing hyperthyroid periodic paralyses to avoid missing a treatable and curable condition.

Adult↗
PubMed1979

[Thyrotoxic periodic paralysis. Report of a case].

A case of thyrotoxic periodic paralysis based on clinical grounds, laboratory data and therapeutic response as well is reported. The authors comment on the differential diagnosis with the most frequent types of periodic paralysis. The importance of a correct diagnosis and treatment as early as possible is stressed as to prevent further development of permanent paralysis due to irreversible degenerative myofibril changes as stated in literature.

Adult↗
PubMedDate not supplied

A case of thyrotropin (TSH)-secreting tumor complicated by periodic paralysis.

A 27-year-old man had symptoms of hyperthyroidism and periodic paralysis. While hyperthyroid, his serum thyrotropin (TSH) level was inappropriately elevated at 6.4 microU/ml. The serum alpha subunit level was also elevated. MR imaging revealed a pituitary tumor and transsphenoidal adenomectomy was performed. Immunocytochemistry with an antibody directed against the beta-subunit of TSH revealed a TSH-secreting tumor. This is the first case of hyperthyroidism due to a TSH-secreting pituitary tumor complicated by periodic paralysis. This association indicates that thyrotoxicosis may induce paralysis in susceptible persons by a mechanism which is not autoimmune.

Adenoma↗
PubMed1977

Vocal cord paralysis: radiologic observations in 21 infants and young children.

The diagnosis of vocal cord paralysis or paresis was made on direct laryngoscopic examination in 34 infants and children during the past 4 years. Twenty-one of the children were first examined radiographically and fluoroscopically, and the initial diagnosis of cord paralysis was suggested by the radiologist. Our experience suggest that vocal cord paralysis or paresis in an infant or young child is not the rare entity previously reported. In more than half of the children the vocal cord dysfuction was of a transient nature. Awareness of the radiographic and fluoroscopic signs that suggest the diagnosis will aid in the early institution of appropriate supportive therapy.

Airway Obstruction↗