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At least 199 records · Page 11Linked to original sources
PubMed2001

Hemidiaphragmatic paralysis increases postoperative morbidity after a modified Fontan operation.

OBJECTIVES: After a Fontan procedure, forward pulmonary blood flow is augmented during inspiration because of negative intrathoracic pressure. Total pulmonary blood flow is higher during inspiration. With hemidiaphragmatic paralysis, inspiratory augmentation of pulmonary flow is lost or diminished. The objective of this study was to compare early postoperative morbidity after the modified Fontan operation in patients with and without hemidiaphragmatic paralysis. METHODS: A case-control analysis was performed comparing 10 patients with documented hemidiaphragmatic paralysis against 30 patients without paralysis who were matched for diagnosis, fenestration, and age. The following early postoperative outcomes were assessed: duration of ventilator support, duration of hospital stay, incidence of ascites, prolonged effusions, and readmission. RESULTS: Preoperatively, there were no significant differences between the 2 groups. However, among the postoperative outcomes, the duration of hospital stay (25.4 +/- 16.6 days vs 10.8 +/- 6.3 days; P =.03), incidence of ascites (70% vs 3%; P <.001), prolonged pleural effusions (60% vs 13%; P =.007), and readmission (50% vs 7%; P =.007) were significantly greater in patients with hemidiaphragmatic paralysis than in those without hemidiaphragmatic paralysis. CONCLUSIONS: Hemidiaphragmatic paralysis after the modified Fontan operation is associated with an increase in early morbidity. Care should be taken to avoid injury to the phrenic nerve. Patients with prolonged effusions should be evaluated for hemidiaphragmatic paralysis.

Case-Control Studies↗
PubMed1986

Vocal cord paralysis and reoperative parathyroidectomy. A prospective study.

One hundred sixty-three patients undergoing reoperative parathyroidectomy were evaluated before and after operation to determine the incidence of, risk factors for, and morbidity of vocal cord paralysis. These patients were compared to 77 patients undergoing initial parathyroid operation, only one of whom had vocal cord paralysis on postoperative indirect laryngoscopy (1.3%). Preoperative examination of the reoperative patients revealed vocal cord paralysis from initial exploration in 11 patients who were excluded from this study. After re-exploration, 10 patients (6.6%) had vocal cord paralysis, eight unilateral and two bilateral. Right vocal cords were paralyzed twice as often as left. In 90%, vocal cord paralysis was associated with removal or biopsy of an ipsilateral gland. Vocal cord paralysis occurred despite intraoperative visualization of the recurrent laryngeal nerves. Preoperative localization, parathyroid gland pathology, and concomitant thyroidectomy were not associated with increased risk of vocal cord paralysis. Hoarseness was the major symptom. Tracheostomy was required for two patients, one was permanent. One patient was treated for aspiration with a temporary gastrostomy. Nine of 10 patients had return of normal voice quality in an average of 4 months time. On examination 4 years or more after surgery, two of five patients had normal vocal cord motion. The oblique anatomic course of the right recurrent laryngeal nerve may account for the greater frequency of right vocal cord paralysis.

Follow-Up Studies↗
PubMed2000

Impact of facial paralysis on patients with acoustic neuroma.

OBJECTIVE: To assess the psychological distress, the ways of coping with that stress, and the self-esteem of patients with facial paralysis after acoustic neuroma surgery. Possible predictors and associations between these measures were also explored. STUDY DESIGN: Four validated questionnaires were completed by patients with facial paralysis after acoustic neuroma surgery: 1) the Derriford Appearance Scale (DAS) to measure psychological distress, 2) the COPE questionnaire to measure how patients cope with facial paralysis, 3) the Personal Report questionnaire to measure the self-esteem of patients, and 4) the Facial Paralysis Questionnaire (FPQ) to measure the severity of facial paralysis. PATIENTS: One hundred three patients with facial paralysis after surgical removal of acoustic tumors. RESULTS: Distress spanned a wide range in these patients. There was no statistically significant association between the level of distress and the grade of facial paralysis or between time since operation and levels of distress. Women had higher levels of distress (P = .02) and a significant negative correlation was found between levels of distress and age (r = -0.28, P = .005). High levels of distress were associated with low levels of self-esteem, as shown by the significant negative correlation between level of distress and self-esteem (r = -0.59, P = .01). A significant correlation between distress and maladaptive coping (r = 0.31, P = .002) was also found. Stepwise multiple regression of the distress scores revealed that self-esteem was the most important contributing factor (standardized coefficient beta -0.60, P = .0001), followed by age (beta -0.24, P = .006) and sex (beta -0.21, P = .04). This model explained 44% of the distress variance. CONCLUSION: Clinicians must be aware of the distress felt by some patients experiencing facial palsy after acoustic neuroma surgery and that the level of distress may not be related to the clinical grade of the facial nerve paralysis. People with low self-esteem, young people, and women suffer from more distress due to the facial palsy. Clinicians should thoroughly counsel patients before and after surgery and should implement measures that increase patients' self-esteem and decrease their distress, especially in these high-risk groups.

Adaptation, Psychological↗
PubMed2001

Unilateral palate paralysis in patients with nasopharyngeal carcinoma: imaging and clinical correlations.

OBJECTIVE: Neck masses, hearing impairment, and blood-tinged nasal discharges are three major clinical manifestations of nasopharyngeal carcinoma (NPC). Because of the relationship between the anatomic structures of the fossa of Rosenmüller and the levator veli palatini muscle, NPC arising in the fossa can invade the levator muscle, limiting movement or causing paralysis of the ipsilateral soft palate. It is well known that NPC originates commonly from the fossa of Rosenmüller. We therefore hypothesize that the clinical signs of unilateral palate paralysis in patients with NPC must be far more common than usually realized. This issue is, as yet, not fully addressed in the literature. STUDY DESIGN: A prospective study of all patients with newly diagnosed NPC. METHODS: Two hundred sixty-four patients with newly diagnosed NPC were studied. Clinical records included the details of their clinical presentations and the results of physical and neurological examinations. The degree of elevation of the soft palate during phonation was carefully evaluated. Magnetic resonance imaging (MRI) of the head and neck region with a particular emphasis on the levator veli palatini muscles was then performed. The degree of paralysis of the palate was correlated with the degree of invasion of the levator muscles by the tumor, as seen with imaging. The incidence of paralysis of the palate in the patients with NPC was also determined. RESULTS: At the time of diagnosis, ipsilateral paralysis of the palate was observed in 137 (52%) of the 264 patients with NPC. The results of imaging indicated that 62% (163 of 264) of the patients had radiological evidence of tumor invasion of the levator muscle. The degree of paralysis of the palate corresponded well to the extent of tumor invasion of the levator muscle. Paralysis of the palate was not evident in 26 patients with early perimuscular infiltration of the levator muscle. CONCLUSION: This study revealed that ipsilateral invasion of the levator veli palatini muscle by NPC is common and typically presents with signs of unilateral palate paralysis. This subtle sign is relatively common in patients with NPC. Consequently, we think palate function should be routinely tested when diagnosing NPC, particularly when the patient has unilateral aural symptoms or a neck lump.

Female↗
PubMed1995

Paralysis caused by acute myelitis in Theiler's murine encephalomyelitis virus strain GD VII infection is induced by CD4+ lymphocytes infiltrating the spinal cord.

Intravenous infection by Theiler's murine encephalomyelitis virus strain GD VII causes acute encephalomyelitis and paralysis in infected mice. However, nude mice and cyclophosphamide-treated ddY mice did not show paralysis when they were able to survive until day 20 post-infection (p.i.). Of ddY mice infected with 5 x 10(7) p.f.u./mouse, 70-80% showed symptoms of paralysis on day 20 p.i. The viral titres in the brain and spinal cord in infected mice were not significantly different between paralytic and non-paralytic mice. In all of the mice infected with the virus, CD4+ lymphocytes and CD8+ lymphocytes had infiltrated the brain on days 10, 12, 14 and 20 p.i. as demonstrated by flow cytometric analysis. In contrast, few T lymphocytes infiltrated the spinal cord in the non-paralytic mice. Administration of an anti-CD4 monoclonal antibody (MAb) or anti-T cell receptor-alpha beta MAb on day 6 p.i. inhibited paralysis until day 20 p.i., though 20% of the MAb-treated mice and 80% of the control mice showed paralysis. Administration of anti-CD8 MAb was not effective in the suppression of paralysis. The MAb treatment did not significantly augment viral replication in the spinal cord, although the viral titres in the brain of the MAb-treated mice increased significantly. After the transfer of spleen cells from infected C3H mice, the recipient mice infected with a small amount of the virus showed paralysis, though uninfected mice did not. This transfer could be blocked by CD4+ lymphocyte depletion of the donor mice. These results indicate that paralysis caused by acute myelitis in Theiler's virus strain GD VII infection is induced by CD4+ lymphocytes infiltrating the spinal cord.

Acute Disease↗
PubMed1991

In vivo and in vitro sodium pump activity in subjects with thyrotoxic periodic paralysis.

OBJECTIVE: To examine whether sodium pump activity plays a part in the pathogenesis of thyrotoxic periodic paralysis. DESIGN: Measurement of platelet sodium-potassium ATPase and in vivo sodium pump activities in healthy subjects and thyrotoxic subjects with and without paralysis. SETTING: University hospital in Hong Kong. SUBJECTS: 21 healthy subjects, 23 untreated thyrotoxic subjects, 13 untreated men with periodic paralysis, seven treated thyrotoxic subjects, and six treated men with periodic paralysis. MAIN OUTCOME MEASURES: Platelet Na+, K(+)-ATPase activity and plasma rubidium concentration after oral loading. RESULTS: Median (range) platelet Na+, K(+)-ATPase activity in thyrotoxic subjects was 253 (169-821) mumol inorganic phosphate/h/g protein--significantly higher than that in healthy subjects (134 (81-180) mumol/h/g protein; p less than 0.001). Na+, K(+)-ATPase activity in those with periodic paralysis was 374 (195-1196) mumol/h/g protein, again significantly higher than that in healthy subjects (p less than 0.001) and that in other thyrotoxic subjects (p less than 0.01) despite similar degrees of hyperthyroidism. Activities in treated thyrotoxic subjects with and without periodic paralysis were 148 (110-234) and 131 (86-173) mumol/h/g protein respectively. Mean (95% confidence interval) plasma rubidium concentration five hours after oral administration in thyrotoxic subjects (7.0 (6.6 to 7.5) mumol/l) was significantly lower than in healthy subjects (10.2 (9.5 to 10.9) mumol/l; p less than 0.001) and higher than in those with periodic paralysis (6.0 (5.7 to 6.3) mumol/l; p less than 0.01). CONCLUSIONS: Sodium pump activity in untreated subjects with periodic paralysis is higher than in other thyrotoxic subjects, and this may be responsible for the hypokalaemia.

Adult↗
PubMed1996

Acute otitis media and facial paralysis in children.

We reviewed 10 children who presented with facial paralysis after the onset of acute otitis media. The objective of the study was to examine the outcome of facial paralysis in children with acute otitis media treated without facial nerve decompression. Two groups were identified: 8 patients with incomplete paralysis and 2 with complete paralysis. Seven of the 8 patients with incomplete paralysis had rapid return of function after myringotomy and intravenous antibiotics. The eighth patient had delayed recovery requiring 9 months before complete return of function. The 2 patients with complete paralysis required mastoidectomy to control otorrhea and fever after initial myringotomy and antibiotics. Both patients had a prolonged recovery requiring 3 and 7 months for complete recovery. Patients with incomplete paralysis generally show rapid improvement following wide myringotomy and antibiotic treatment. A more protracted recovery may be expected in patients with complete paralysis; excellent return of function is expected when mastoidectomy without facial nerve decompression is employed.

Acute Disease↗
PubMed1998

Immunologic aspects of facial nerve paralysis induced by herpes simplex virus infection in mice.

This immunologic aspects of facial nerve paralysis due to herpes simplex virus type 1 (HSV-1) infection were investigated in a mouse model system. Half of the 4- to 5-week-old mice developed facial nerve paralysis, whereas none of the 6-week-old mice died or developed facial nerve paralysis on inoculation with HSV-1. Six-week-old mice showed significantly higher titers of anti-HSV-1 neutralizing antibody than did 4-week-old animals. Passive transfer of either anti-HSV-1 antibody or HSV-1-immunized splenic T cells into 4-week-old mice 3 hours after HSV-1 inoculation prevented development of facial nerve paralysis and death, whereas such transfers 48 or 96 hours after HSV-1 inoculation did not prevent or exacerbate facial nerve paralysis. These results demonstrate that the age and the immunologic potency of mice are closely related to the pathogenesis of facial nerve paralysis. That facial nerve paralysis developed even in 6-week-old mice whose T-cell function was suppressed with anti-CD3 antibody suggests that virus-induced cellular demyelination is unlikely as a cause of facial nerve paralysis in this animal model.

Age Factors↗
PubMed1994

Paramyotonia congenita without cold paralysis: a case report.

A 27-year-old-woman with paramyotonia congenita was reported. She began to suffer from myotonia since infancy. Myotonia was aggravated by cold, but with intense cooling myotonia did not change to flaccid paralysis. Four generations of her family showed the same symptoms that suggested autosomal dominant inheritance. Neurological examinations revealed no impairments of mental function, cranial nerves and sensory system. Muscular atrophy or hypertrophy was not observed. Percussion myotonia of the tongue and thenar muscles could be elicited at room temperature. Myotonia was aggravated by cold. An oral intake of potassium chloride (7 grammes) did not provoke any muscle weakness or flaccid paralysis. Routine laboratory data and findings of head CT scan, cerebrospinal fluid and electroencephalogram were normal. The nosological distinction between paramyotonia congenita and hyperkalemic periodic paralysis has been debated since 1956. Paralysis induced by cold is thought to be a feature of paramyotonia congenita, thus raising a possible relationships to hyperkalemic periodic paralysis. In our case cold paralysis never occurred spontaneously and could not be provoked by immersion in ice water or by potassium loading. This finding confirms the existence of paramyotonia congenita without cold paralysis and may provide a nosological distinction between paramyotonia congenita and hyperkalemic periodic paralysis.

Adult↗
PubMed1998

[An assessment of physical and psychological stress of patients with facial paralysis].

The purpose of this study was to determine if there is a relationship between the appearance of facial paralysis and physical or psychological stress. Subjects were 55 patients (23 men, 32 women) with facial paralysis (32 with Bell's palsy, 23 with Ramsay Hunt syndrome) who visited the Department of Otolaryngology, Nihon University Itabashi Hospital, from August 1994 to March 1996. At the time of the initial visit, patients were asked if they had any physical or psychological stress one week before the occurrence of facial paralysis. The degree of psychological stress was rated by Niina's Psychological Stress Response Scale 50 Items Revised (PSRS-50R). Answers were obtained from 52 of the 55 subjects. Forty patients (76.9%) reported that they had felt physically fatigued, suggesting some type of relationship between the occurrence of facial paralysis and physical stress. Twenty-seven patients (51.9%) reported the existence of psychological stress. However, the evaluation of psychological stress by PSRS-50R did not reveal a high level of psychological stress in any patient, indicating lack of a strong relationship between the occurrence of facial paralysis and psychological stress. Stepwise regression analyses were made to study the relationship between the degree of paralysis at the time of the initial visit and factors which affect the prognosis of the paralysis. Those patients who reported physical fatigue before the appearance of facial paralysis had more abnormal values on the nerve excitability test than those who did not report such fatigue.

Adolescent↗
PubMed1992

Bilateral facial paralysis: a case presentation and literature review.

Bilateral facial paralysis is a diagnostic challenge, which may manifest itself as either a simultaneous or alternating form, occurring in 0.3-2.0% of patients that present with facial paralysis. The differential diagnosis of facial paralysis includes congenital, traumatic, neurologic, infectious, metabolic, neoplastic, toxic, iatrogenic and idiopathic etiologies. While idiopathic facial paralysis is the most common diagnosis, a comprehensive evaluation must be completed prior to this diagnosis in patients with bilateral facial paralysis. A representative case of simultaneous bilateral facial paralysis is presented. The literature is reviewed and discussed. A diagnostic protocol for the evaluation of bilateral facial paralysis is proposed. Bilateral facial paralysis requires a thorough evaluation and may prove to be a diagnostic dilemma.

Aged↗
PubMed2005

Surveillance of acute flaccid paralysis in Hong Kong: 1997 to 2002.

OBJECTIVES: To describe the characteristics of patients reported with acute flaccid paralysis between 1997 and 2002, and to evaluate the performance of the acute flaccid paralysis surveillance system using indicators recommended by the World Health Organization. DESIGN: Retrospective study. SETTING: Department of Health, Hong Kong. PARTICIPANTS: Children aged younger than 15 years who were reported to the Department of Health between 1997 and 2002 with acute flaccid paralysis. RESULTS: Of 120 children with acute flaccid paralysis reported between 1997 and 2002, 42% were younger than 5 years of age. None of the cases were acute poliomyelitis or polio-compatible. A neurological cause was identified in 67.5% of cases, of which the most common was Guillain-Barre syndrome (42%), followed by transverse myelitis (15%). All except one of the performance indicators consistently met World Health Organization requirements and thus demonstrated the effectiveness of the acute flaccid paralysis surveillance programme. The acute flaccid paralysis notification rate consistently exceeded 1.0 per 100 000 population below 15 years of age. The requirement for adequate stool investigation was the single indicator that did not satisfy World Health Organization requirements. This highlighted the importance of maintaining physicians' awareness of acute flaccid paralysis surveillance. CONCLUSION: Hong Kong should remain vigilant for acute flaccid paralysis. The effective surveillance system and its evaluation may serve as a model for surveillance of other infectious diseases.

Acute Disease↗
PubMed1996

The effect of single-dose and continuous skeletal muscle paralysis on respiratory system compliance in paediatric intensive care patients.

OBJECTIVE: To investigate the effect of single dose and continuous skeletal muscle paralysis on respiratory system compliance in 53 paediatric intensive care patients. DESIGN: Prospective clinical study. SETTING: Multidisciplinary paediatric intensive care unit. PATIENTS: Twenty-three children ventilated for acute pulmonary pathology, and 30 ventilated for isolated intracranial pathology, who initially had normal lungs. INTERVENTIONS: The 23 patients with acute pulmonary pathology received a single dose of muscle relaxant to facilitate diagnostic procedures. Fifteen patients with isolated intracranial pathology received continuous skeletal muscle paralysis for longer than 24 h, and the other 15 received no paralysis. MEASUREMENTS AND RESULTS: Respiratory system compliance deteriorated by 14% from 0.519 +/- 0.2 to 0.445 +/- 0.18 ml cmH2O-1 kg-1 (p < 0.001) following a single dose of muscle relaxant in the 23 patients with acute pulmonary pathology. In the 15 with isolated intracranial pathology who received continuous skeletal muscle paralysis there was a progressive deterioration in compliance, which reached 50% of the initial compliance by day 4 of paralysis (p < 0.001) and improved back to normal following discontinuation of paralysis. There were no changes in compliance in the 15 patients with isolated intracranial pathology who were ventilated but not paralysed. The paralysed patients required mechanical ventilation longer than the non-paralysed patients (p < 0.001), and 26% of these patients developed nosocomial pneumonia (p = 0.03), a complication that was not seen in the non-paralysed patients. CONCLUSIONS: Skeletal muscle paralysis results in immediate and progressive deterioration of respiratory system compliance and increased incidence of nosocomial pneumonia. The benefits of paralysis should be balanced against the risks of deteriorating pulmonary function.

Acute Disease↗
PubMed1990

Cation transport across lymphocyte plasma membranes in euthyroid and thyrotoxic men with and without hypokalaemic periodic paralysis.

1. To study potassium transport in hypokalaemic periodic paralysis in a model of striated muscle cells, we measured specific [3H]ouabain binding (the number of sodium-potassium pumps), sodium-potassium-pump-mediated (ouabain-sensitive) 86Rb+ influx and sodium-potassium-pump-independent (ouabain-resistant) 86Rb+ influx in lymphocytes in vitro. 2. The subjects comprised euthyroid and thyrotoxic men with hypokalaemic periodic paralysis between attacks, men with uncomplicated thyrotoxicosis, and healthy men matched for age and weight. 3. Thyrotoxic patients, both with and without periodic paralysis, had significantly more lymphocyte sodium-potassium pumps than normal, and a significantly greater sodium-potassium-pump-mediated 86Rb+ influx. Anti-thyroid treatment corrected this defect in patients with thyrotoxic periodic paralysis. Euthyroid patients with cryptogenic periodic paralysis had significantly increased sodium-potassium-pump-mediated 86Rb+ influx, but a normal number of sodium-potassium pumps. 4. Only untreated thyrotoxic and euthyroid patients with periodic paralysis showed a significant increase in sodium-potassium-pump-independent 86Rb+ influx (5.2 +/- 2.8 and 4.5 +/- 1.8 respectively, vs control 2.8 +/- 1.0 pmol h-1 10(-6) cells; mean +/- SD; P less than 0.001, P less than 0.005). 5. We conclude that thyrotoxicosis increases the number and activity of sodium-potassium pumps and facilitates, but is probably not necessary for, periodic paralysis. Hypokalaemic periodic paralysis is associated with an increase in sodium-potassium-pump-independent potassium influx.

Adult↗
PubMed2006

Clinical review: Thyrotoxic periodic paralysis: a diagnostic challenge.

CONTEXT: The aim of this article was to review the clinical presentation, pathogenesis, and management of thyrotoxic periodic paralysis (TPP). EVIDENCE ACQUISITION: A MEDLINE search was conducted for articles published during the last 40 yr based on the key words thyrotoxic periodic paralysis and hypokalemic periodic paralysis. A total of 281 primary articles and 168 references of the retrieved articles were also reviewed. EVIDENCE SYNTHESIS: TPP is a common complication of hyperthyroidism in Asian men but is increasingly seen in Western countries. Hypokalemia and muscle paralysis results from a sudden intracellular shift of potassium and is not due to potassium deficiency. Clinical features of hyperthyroidism in patients with TPP may be subtle. Immediate potassium supplementation prevents serious cardiopulmonary complications and may hasten the recovery of muscle weakness. Nonselective beta-adrenergic blockers can ameliorate and prevent recurrence of the paralytic attacks. This episodic paralysis will remit with definitive control of hyperthyroidism. Increased sodium-potassium ATPase pump activity and enhanced insulin response in patients with TPP is postulated to contribute to the hypokalemia. The genetic predisposition for TPP is not entirely clear. Association of polymorphisms of the calcium channel alpha1-subunit gene with TPP has been noted. CONCLUSIONS: Due to population mobility, TPP is increasingly common in Western countries. Early diagnosis and prompt treatment prevent life-threatening complications associated with hypokalemia and muscle weakness. Assaying of thyroid function in patients with hypokalemic paralysis distinguishes TPP from other forms of hypokalemic periodic paralysis.

Antithyroid Agents↗
PubMed1986

[Consequences of adult brachial plexus paralysis and its surgical treatment on respiratory function].

The authors have studied 22 patients suffering from traumatic brachial plexus injuries and the consequences on respiratory function of paralysis of the diaphragm and other respiratory muscles. They have also studied the effects of some surgical treatment on respiratory function. The patients were divided into three groups: post-traumatic paralysis of the diaphragm (5 cases), patients who had had an intercostal neurotization (11 cases) and patients with paralysis of some respiratory muscles with an intact diaphragm (2 cases). Six tests were performed--vital capacity, total pulmonary capacity, residual functional capacity, airway resistance, maximum expiratory volume per second and airflow at 50 p. 100 of the vital capacity. Respiratory function was decreased by about 50 p. 100 in cases of diaphragmatic paralysis. This finding should be taken into consideration in cases of extensive lesions of the brachial plexus. The effects of intercostal neurotization were minimal when performed in cases with respiratory paralysis, but with an intact diaphragm. They were negligible in the absence of any respiratory paralysis. It is concluded that intercostal neurotization should not be performed in cases with diaphragmatic paralysis. In such cases, other types of neurotization are preferred.

Adolescent↗
PubMed1999

Cisplatin induced reversible bilateral vocal cord paralysis: an undescribed complication of cisplatin.

BACKGROUND: Bilateral vocal cord paralysis is uncommon. Most cases occur secondary to trauma, malignancy, surgery, or intubation. Also, it was reported as a side effect of Vinca alkaloids. METHODS: We report a patient with small cell lung cancer who developed bilateral vocal cord paralysis and needed to be intubated after treatment with cisplatin and etoposide. All workups excluded metastases as a cause of bilateral vocal cord paralysis. The patient required tracheostomy; she did not receive any further chemotherapy. After 11 weeks, vocal cord paralysis disappeared, tracheostomy was reversed, and the patient remained symptom free; however, 6 months later, the patient developed brain and liver metastases and died from her disease with no evidence of vocal cord paralysis. RESULTS: We report a case of reversible bilateral vocal cord paralysis that we believe to be secondary to cisplatin toxicity, which is an undescribed complication of this drug. CONCLUSION: Cisplatin can induce reversible bilateral vocal cord paralysis. The concurrent use of cisplatin and etoposide might have contributed to this complication in our patient.

Aged↗
PubMedDate not supplied

Immediate post-dosing paralysis following severe soman and VX toxicosis in guinea pigs.

There have been numerous studies of the central nervous system (CNS) involvement in organophosphate (OP) poisoning showing status epilepticus and/or 'electrographic seizures'. Brain damage has been demonstrated as 'neuronal necrosis' primarily in the cortex, thalamus and hippocampus. To the authors' knowledge there have been no reports of partial/total paralysis following close upon OP exposure although delayed paralysis has been reported. This report summarizes the immediate, OP induced paralytic events recorded in guinea pigs during development of the Canadian reactive skin decontaminant lotion (RSDL). As part of the development work, supra-lethal cutaneous doses of OP were applied to large numbers of guinea pigs followed by decontamination with the RSDL or predecessor lotions and solvents. Soman (pinacolyl methylphosphonofluoridate; GD) challenges were applied to 1277 animals and S-(2-diisopropyl-aminoethyl) methylphosphorothiolate (VX) challenges to 108. The classic sequence of clinical signs--ptyalism, tremors, fasciculations, convulsions, apnea and flaccid paralysis before death--was seen in the 658 animals that died and in many of the survivors. Eighty-four of 688 survivors of GD and 4 of 39 survivors of VX showed random paralysis of various distal regions following recovery from an insult which produced convulsions and/or flaccid paralysis. Because the experiments were designed to assess the decontamination procedures, there were no apparent relationships between the amounts of OP applied and the sequellae recorded. The observations of paralysis were also incidental to the prime focus of the experiments. Because of this, only ten animals paralysed following GD exposure were examined for histological effects. The pathologist diagnosed 'encephalomalacia' and 'focal necrotic lesions' in the cerebral cortex and 'focal necrotic lesions' in one spinal cord. Of the 84 guinea pigs paralysed after GD challenge, one was not decontaminated and the decontaminants used on the remainder were sufficiently varied that there appeared to be no relationship between the type of decontaminant and the resulting paralysis.

Animals↗