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PubMed2002

Segmental motor paralysis after expansive open-door laminoplasty.

STUDY DESIGN: A retrospective study was conducted to investigate patients in whom segmental motor paralysis developed after expansive open-door laminoplasty for cervical myelopathy. OBJECTIVE: To propose the involvement of the spinal cord as a possible mechanism in the development of segmental motor paralysis. SUMMARY OF BACKGROUND DATA: Segmental motor paralysis is seen occasionally in patients who undergo expansive open-door laminoplasty for cervical myelopathy, and has long been attributed to nerve root lesions caused by either traumatic surgical techniques or a tethering effect induced by excessive posterior shift of the spinal cord after decompression. Involvement of spinal cord pathology is not suggested in the English literature. METHODS: The study group consisted of 15 patients (11 men and 4 women) in whom postoperative segmental motor paralysis developed after expansive open-door laminoplasty during a minimum follow-up of 2 years. Their average age at the time of surgery was 56 years. Characteristics of the paralysis, clinical symptoms, recovery rates calculated using pre- and postoperative Japanese Orthopedic Association scores, and radiographic findings including pre- and postoperative magnetic resonance images were analyzed retrospectively and compared with those of 126 patients without segmental paralysis who underwent expansive open-door laminoplasty. RESULTS: The paralysis occurred mainly, but not only, at C5, and eight patients had multilevel involvements predominantly in the hinge side, whereas two patients had paralysis on both sides. The paralysis had developed after an average of 4.6 days. Of the 15 patients, 14 reported severe numbness or dysesthesia in their hands before surgery, and their average recovery rate for upper extremity sensory disturbance was lower than for those without paralysis. Postoperative magnetic resonance imaging showed the presence of a T2 high-signal intensity zone in the spinal cord of all the patients. The level of such abnormal signal areas corresponded to the level of paralyzed segments in 10 of the 15 patients. Paralysis resolved completely in 11 patients. CONCLUSIONS: Delayed onset of paralysis, dysesthesiain the upper extremities, and the presence of T2 high-signal intensity zones suggest that a certain impairment in the gray matter of the spinal cord may play an important role in the development of postoperative segmental motor paralysis.

Adult↗
PubMed2004

A new clinical evaluation for hysterical paralysis.

STUDY DESIGN: A cross-sectional study was performed to elucidate the usefulness of a new clinical evaluation, and a prospective study was performed to detect hysterical paralysis using this evaluation method. OBJECTIVES: To make a correct diagnosis of hysterical paralysis, a new clinical evaluation was developed. SUMMARY OF BACKGROUND DATA: Hysterical paralysis is a conversion disorder. Its diagnosis must be ruled out when encountering a patient with paralysis, therefore imaging and electrophysiological studies are often necessary, but costly. The principal salient diagnostic features for diagnosing hysterical paralysis are thought to be the preservation of a normal reflex pattern, normal rectal sensation, and normal bladder and bowel functions; however, these features are not always successfully identified. METHODS: A new clinical evaluation named the "Spinal Injuries Center" test was developed. The lower extremities of the patients were divided into two groups as follows: in group A, the patients were able to lift up the knee; in group B, the patients were unable to lift up the knee. The 96 legs of the 48 patients who had obvious myelomalacia were randomly chosen. All legs were investigated using the Spinal Injuries Center test, and the association between each group and the Spinal Injuries Center test was examined. The 28 legs of the 14 patients in whom hysterical paralysis was diagnosed were prospectively evaluated using the Spinal Injuries Center test, and the association between the groups and the Spinal Injuries Center test was examined. RESULTS: Forty-eight legs were classified as group A, and 48 legs were classified as group B. In group A, 45 legs were judged to be positive for the Spinal Injuries Center test, and 3 legs were negative. In group B, 1 leg was judged to be positive for the Spinal Injuries Center test, and 47 legs were negative. All legs of the patients with hysterical paralysis were classified as group B; however, all legs were positive for the Spinal Injuries Center test. CONCLUSIONS: The Spinal Injuries Center test is a new clinical evaluation method that can help make a correct diagnosis of hysterical paralysis. When a patient is unable to lift up his knees by himself, the result of the Spinal Injuries Center test is considered to be positive, and hysterical paralysis is diagnosed in such patients. The diagnosis of hysterical paralysis must be ruled out when encountering patients with paralysis, and as a result, imaging and electrophysiological studies are often necessary. Unfortunately, such tests are costly. Thus, a new clinical evaluation for the diagnosis of hysterical paralysis, named the Spinal Injuries Center test, was developed. When patients who are unable to lift up their knees by themselves test positive using the Spinal Injuries Center test, then they are considered to have ether hysterical or simulated paralysis.

Adolescent↗
PubMed2004

Evaluation of recurrent nerve paralysis due to thoracic aortic aneurysm and aneurysm repair.

OBJECTIVES: We sought to clarify the relationship between the outcome of recurrent laryngeal nerve paralysis with the characteristics of the thoracic aortic aneurysm and the surgical procedure used in each patient. METHODS: Nine patients who developed recurrent nerve paralysis (nonsurgical paralysis) due to a thoracic aortic aneurysm alone and 14 patients who underwent artificial vessel replacement for thoracic aortic aneurysm and developed recurrent nerve paralysis postoperatively (surgical paralysis) were evaluated. RESULTS: In the patients with nonsurgical paralysis, the aneurysms were similar in size to those of other patients who underwent surgery of the thoracic aorta and were invariably located near the aortic arch. Aneurysm shape was not associated with nerve paralysis. Surgical paralysis was alleviated in two patients. Surgical paralysis was observed in 9% of those who underwent surgery of the thoracic aorta. Vocal cord mobility recovered in 4 of the 11 patients with surgical paralysis who underwent follow-up. Symptoms were alleviated by rehabilitation in many patients who did not recover vocal cord mobility. The positions of the artificial vessel anastomoses are thought to be closely related to the outcome of paralysis. CONCLUSION: Recurrent nerve paralysis reduced not only the patient's quality of life but also survival by leading to disorders including aspiration pneumonia. Therefore, early rehabilitation should be performed, and surgical treatment should be considered, if necessary, for patients with recurrent nerve paralysis.

Adult↗
PubMed1997

[Clinical classification of ALS patients based on the total course of ALS--proposal of respiratory motor paralysis-preceded type and its significance].

Since the motor paralysis occurs in all motor systems in ALS, the clinicopathological findings and care of the patients living beyond the development of respiratory failure must be considered. We have divided the efferent motor systems into four groups, i.e., limb, bulbar, respiratory, and external ocular. In this study, 37 ALS patients were followed for more than two years with respirator, and the onset of motor paralysis in all four systems was observed in each patient. First, we classified the patients into three groups according to the number of paralyzed motor systems observed within six months from the onset of the first motor paralysis, and we discuss the patient's prognosis after the first motor paralysis. Twenty-one patients with paralysis of the respiratory motor system alone were categorized as respiratory paralysis-preceded type ALS (R-type ALS), four patients with paralysis of the bulbar motor system alone as bulbar paralysis-preceded type ALS (B-type ALS), and 12 patients with simultaneous paralysis of two or more motor systems as combined motor system paralysis type ALS (C-type ALS). The results showed that the prognosis of R-type ALS is slow progression and that of C-type ALS, rapid progression. Next, we investigated the time of occurrence of the first motor paralysis of the four motor systems in 37 patients, and we discuss the most vulnerable motor functions in ALS, i.e., the initial clinical presentations in ALS. The most frequent first motor paralysis was of the respiratory motor system, and the initial clinical manifestations in ALS were impairment of fine discriminating voluntary respiratory and limb motor functions. These findings could be explained by the rule of ALS involvements, according to which onto-genetically newer motor functions are lost earlier than the older ones. Based on the findings in this study, we concluded that ALS initially involves the ontogenetically new motor functions in "the first system" proposed by G. Holstege, whose anatomical structure is composed of pre-motoneurons and motoneurons in the brain stem and spinal cord.

Adolescent↗
PubMed1984

The effect of paralysis on oxygen consumption in normoxic children after cardiac surgery.

To determine whether paralysis reduces oxygen consumption (V02) after cardiac surgery in infants, the authors measured V02 before and after paralysis in 17 sedated infants who were ventilated mechanically after cardiac surgery. Oxygen consumption was determined as being the difference between oxygen content of inspired and expired gases. The absence or presence of "movement" (breathing or repeated movement of the extremities) before paralysis was noted. For eight infants who did not "move" before paralysis, VO2 was similar before (9.1 +/- 1.2 ml . kg-1 . min-1, mean +/- SD) and after (9.0 +/- 1.5 ml . kg-1 . min-1) paralysis (P = 0.81). However, for nine infants who did "move" before paralysis, VO2 decreased from 9.2 +/- 1.4 ml . kg-1 . min-1 before paralysis to 8.0 +/- 1.4 ml . kg-1 . min-1 after paralysis (P less than 0.05). One infant in each group had an increase in VO2 greater than 10% of the baseline value (i.e., 12% and 14%). In conclusion, if breathing or repeated movement is present before paralysis, paralysis decreases VO2 by 13% in sedated infants after cardiac surgery. If repeated or regular movement is not present before paralysis, paralysis does not decrease VO2. These data suggest that in normoxic patients, muscle paralysis does not significantly alter V02 and therefore should not be used for this purpose.

Anesthesia↗
PubMed1996

Normal insulin release during sustained hyperglycaemia in hypokalaemic periodic paralysis: role of the potassium channel opener pinacidil in impaired muscle strength.

1. Hypokalaemic periodic paralysis is characterized by attacks of muscle weakness. Glucose, insulin and an abnormal regulation of ATP-sensitive potassium channels may be involved in these attacks. We studied the effect of hyperglycaemia and of the potassium channel opener pinacidil on insulin release and muscle strength in patients with hypokalaemic periodic paralysis. 2. Insulin release was assessed on two occasions in four patients with hypokalaemic periodic paralysis and in eight matched control subjects, with and without treatment with 25 mg pinacidil orally, during a hyperglycaemic glucose clamp at a blood glucose level of 10 mmol/l, in a placebo-controlled, double-blind study. Muscle strength was measured in the hypokalaemic periodic paralysis patients before and during hyperglycaemia using a handheld dynamometer. 3. During the clamp, the mean glucose concentration (10-180 min) in control subjects was 9.9 +/- 0.07 and 10.0 +/- 0.03 mmol/l with and without pinacidil respectively, and in patients with hypokalaemic periodic paralysis was 10.0 +/- 0.04 and 10.1 +/- 0.06 mmol/l respectively (not significantly different). In both groups, the areas under the insulin curve from 0 to 10 min (first-phase insulin release) and from 30 to 180 min (second phase) were not different on the pinacidil study day compared with on the placebo day. The areas under the insulin curve of the first and second phases also did not differ between control subjects and patients with hypokalaemic periodic paralysis (with or without pinacidil). The M/I ratio, a measure of insulin sensitivity, was not different in the two groups. On the placebo day, baseline muscle strength in patients with hypokalaemic periodic paralysis was 165 +/- 16 N for the hip abductors and 168 +/- 19 N for the knee flexors. During the period of hyperglycaemia on the placebo day, muscle strength did not decrease in either muscle group. On the pinacidil study day, an increase in muscle strength was found only in the two hypokalaemic periodic paralysis patients with the lowest mean muscle strength (< 150 N) on the placebo day. The two hypokalaemic periodic paralysis patients with a mean muscle strength on the placebo day > 150 N showed no increase in muscle strength with pinacidil. 4. Insulin secretion and sensitivity were normal in patients with hypokalaemic periodic paralysis. Hyperglycaemia during hyperglycaemic clamping did not provoke paralytic attacks and did not result in a decrease in muscle strength. The potassium channel opener pinacidil had no effect on insulin secretion in hypokalaemic periodic paralysis patients or in normal subjects. Pinacidil may enhance muscle strength in those hypokalaemic periodic paralysis patients who suffer partial paralytic attacks.

Adult↗
PubMed1993

Respiratory sensations, cardiovascular control, kinaesthesia and transcranial stimulation during paralysis in humans.

1. To determine whether discomfort associated with breathing (dyspnoea) is related to the chemical drive to breath, three subjects were totally paralysed while fully conscious. Subjective responses to a rising CO2 stimulus were obtained during rebreathing, rebreathing with CO2 added, and breath holding. Dyspnoea was measured with a 10-point Borg scale. 2. Following nasotracheal intubation and ventilation (oxygen saturation, O2,Sat, 98-100% and end-tidal CO2, PET,CO2, 30-40 mmHg), total neuromuscular blockade was induced by a rapid injection of atracurium (> 2.5 mg kg-1) and complete paralysis was maintained with an infusion (5 mg (kg h)-1). Paralysis was confirmed by abolition of the compound muscle action potentials of both the diaphragm and abductor hallucis evoked by supramaximal electrical stimulation of the relevant nerves. Communication via finger movement was preserved for the first 20-30 min following paralysis by inflation of a sphygmomanometer cuff on one arm. 3. Before and during complete paralysis, dyspnoea increased progressively during hypercapnia produced by rebreathing (with or without CO2 added to the circuit at 250 ml min-1). The mean PET,CO2 eliciting 'severe' dyspnoea was 46 mmHg during rebreathing, 42 mmHg during 'breath holding', and 52 mmHg during rebreathing with added CO2. There were no significant differences between the values obtained during paralysis and in the control study immediately before paralysis. The duration of breath holding was not prolonged by paralysis and the PET,CO2 at the 'break point' was not altered by paralysis. 4. Thus, dyspnoea is preserved following total neuromuscular blockade. This suggests that chemoreceptor activity, via the central neuronal activity which it evokes, can lead to discomfort in the absence of any contraction of respiratory muscles. 5. During paralysis, attempted contraction of arm, leg and trunk muscles increased heart rate and blood pressure. For attempted handgrip contractions, the increases in heart rate (range, 7-15 beats min-1) and mean arterial pressure (range, 20-32 mmHg) were similar to those recorded with actual contractions in trials immediately before paralysis. In one subject, graded increases in heart rate and blood pressure occurred for attempted contractions of 45 s duration over a range of intensities (0-100% maximal effort). 6. During complete paralysis, transcranial electromagnetic stimulation of the motor cortex produced illusory twitch-like movements of the wrist and digits. This also occurred in separate studies during complete ischaemic paralysis and anaesthesia of the forearm and hand.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2006

Vocal cord paralysis after aortic arch surgery: predictors and clinical outcome.

OBJECTIVE: This study is retrospective cohort study of data on vocal cord paralysis after aortic arch surgery collected during 14 years at a general hospital. We investigated factors in the development of vocal cord paralysis after aortic arch surgery and the effect of vocal cord paralysis on clinical course and outcome. METHODS: We reviewed data for 182 patients who underwent aortic arch surgery for aortic arch aneurysm and aortic dissection between 1989 and 2003, of whom 58 patients had proximal aortic repair, 62 had distal arch repair, and 62 had total arch repair. We assessed factors associated with the development of vocal cord paralysis and examined in detail the clinical outcome of patients with vocal cord paralysis. RESULTS: Postoperative vocal cord paralysis occurred in 40 patients. Multiple logistic regression analysis revealed the following risk factors with odds ratios (OR) for vocal cord paralysis: extension of procedures into distal arch (OR, 17.0), chronic dilatation of the aorta at the left subclavian artery (OR, 9.14), and total arch repair (OR, 4.24). Adoption of open-style stent-grafts reduced the incidence of vocal cord paralysis (OR, 0.031). The postoperative occurrence of vocal cord paralysis itself emerges as an independent predictor of pulmonary complications (OR, 4.12) and leads to a longer duration of hospital stay. CONCLUSIONS: The risk of vocal cord paralysis after aortic arch surgery depends on surgical factors, such as aneurysmal involvement of the distal arch, or the application of newer, less invasive surgical procedures. Vocal cord paralysis after aortic arch surgery itself, under aggressive postoperative respiratory management, did not increase aspiration pneumonia but was associated with postoperative complications leading to higher hospital mortality and prolonged hospitalization.

Age Distribution↗
PubMedDate not supplied

Lyme borreliosis and facial paralysis--a prospective analysis of risk factors and outcome.

PURPOSE: To evaluate the incidence of Lyme borreliosis in patients with acute idiopathic facial paralysis with special emphasis on the risk factors that explain the poor outcome of facial paralysis and occurrence of Lyme borreliosis. MATERIALS AND METHODS: During a 2-year period, we prospectively studied 503 consecutive patients with acute idiopathic facial paralysis for the presence of Lyme borreliosis. We screened the patients for antibodies to Borrelia burgdorferi and for symptoms or signs related to Lyme borreliosis. Chi-square and logistic regression tests were used for the statistical analysis. Special attention was paid to strict criteria for the diagnosis of Lyme borreliosis. RESULTS: Eleven (2.2%) of the 503 patients with facial paralysis had Lyme borreliosis. Fever, headache, pharyngalgia, enlarged cervical lymph nodes, bilateral paralysis, and arthralgia were more common in patients with Lyme borreliosis than in those without it. In the logistic regression modeling the best combination of explanatory variables for predicting the occurrence of Lyme borreliosis included summer season at the onset of facial paralysis, presence of enlarged cervical lymph nodes, and arthralgia. The best combination of explanatory variables to predict the poor outcome of facial paralysis was total paralysis of facial nerves, recurrent facial paralysis, and hyperacusis. CONCLUSIONS: Lyme borreliosis is an important infectious cause of facial paralysis. In our study, 11 of 503 patients with acute idiopathic facial paralysis had Lyme borreliosis. The screening for serum antibodies in addition to the thorough evaluation of the history of the patient and of the patient's clinical signs or symptoms possibly linked with Lyme borreliosis, are essential when diagnosing Lyme borreliosis.

Acute Disease↗
PubMed1996

[Immunological determinants and the spread of viral infection in facial nerve paralysis induced by herpes simplex virus in mice].

Herpes simplex virus type 1 (HSV-1) infection of the facial nerve has been strongly suggested as a cause of Bell's palsy. The author's group have produced a transient and homolateral facial paralysis in Balb/c mice by inoculating HSV-1 onto the auricle, simulating the symptoms of Bell's palsy. To clarify whether and how age and specific immunity against HSV-1 are involved in the pathogenesis of facial nerve paralysis, age dependent susceptibility to the virus and passive immunization with anti-HSV-1 antibody or immunized splenic T cells were investigated in a mouse model system. Following inoculation of HSV-1 into 3-week-old mice, 80% of the animals died whereas only 13% of 4-to 5-week-old mice died, and 50% developed facial nerve paralysis 1 week after the inoculation. No 6-week-old mice died and 6% developed facial nerve paralysis. Although all mice showed seroconversion of neutralizing antibody regardless of the presence of facial nerve paralysis, six-week-old mice and 4-week-old mice without facial nerve paralysis produce higher titers of anti-HSV-1 antibody than 4-week-old-mice with facial nerve paralysis. These results suggested that the age and the immunological potential of mice are closely related to the pathogenesis of facial nerve paralysis. Passive transfer of either anti-HSV-1 antibody or HSV-1 immunized splenic T cells into 4-week-old mice prevented development of facial nerve paralysis and death if they were transferred within 3 hours postinoculation. However, a similar transfer 48 or 96 hours after HSV-1 inoculation did not produce such protection. HSV-1 DNAs were detected in the facial nerve as early as 48 hours postinoculation by polymerase chain reaction (PCR). These results indicate that the passive immunization, providing both cellular and humoral immunity, is effective for preventing facial nerve paralysis if performed before virus infects the facial nerve. The nervous system has a blood-nerve barrier (BNB) which privileges it from the peripheral immune system. Therefore, once the virus infects the facial nerve, passive immunity transferred from peripheral vessel might be excluded from the virus or virus-infected cells unless the BNB is broken down. Bell's palsy is thought to occur during the course of HSV-1 latency in the geniculate ganglion. If we could reactivate latently infected virus and produce facial nerve paralysis again in the animal model, this might provide clues to clarify not only the pathological mechanism of Bell's palsy but also the interaction between immune system and virus reactivation.

Age Factors↗
PubMed1986

Total facial nerve decompression in recurrent facial paralysis and the Melkersson-Rosenthal syndrome: a preliminary report.

Recurrent facial paralysis is an infrequent problem for the otolaryngologist. This paralysis may be associated with the Melkersson-Rosenthal syndrome, a triad of recurrent facial paralysis, relapsing facial edema, and associated fissured tongue. Most patients do not have the accompanying stigmata of this syndrome. This paralysis may occur unilaterally or bilaterally. The usual sequelae of recurrent facial paralysis are progressive synkinesis and increasing residual paresis with each episode, and total facial paralysis may be the final outcome. Two patients, one with unilateral Melkersson-Rosenthal syndrome and the other with a bilateral recurrent idiopathic facial paralysis, were treated with combined transmastoid and middle cranial fossa total facial nerve exposure, decompression, and slitting of the fibrous nerve sheath. Postoperatively they have not suffered from facial paralysis during a follow-up period of three years. It appears that this surgical management safely and effectively prevents recurrent facial paralysis unilaterally or bilaterally, whether or not it is associated with the Melkersson-Rosenthal syndrome. Until further experience with this particular management of recurrent facial paralysis is reported, however, caution should be used in recommending it. Additionally, it should not be assumed from this experience that surgical treatment for idiopathic facial paralysis in Bell's palsy is necessarily implied.

Adolescent↗
PubMed2003

Effects of acyclovir on facial nerve paralysis induced by herpes simplex virus type 1 in mice.

OBJECTIVES: Bell's palsy has recently been claimed to be caused by herpes simplex virus type 1 (HSV-1) infection. The anti-viral agent acyclovir is a specific inhibitor of herpesvirus replication, and the most effective agent for the treatment herpesvirus infection. The purpose of this experiment was to assess the effect of acyclovir on the facial nerve paralysis included by HSV-1 infection. METHODS: We succeeded in producing an animal model of acute and transient facial nerve paralysis induced with HSV-1 neuritis simulating human Bell's palsy. In this study, acyclovir administration was performed before and after facial nerve paralysis, and continued for 5 days. Controls were given phosphate-buffer saline (PBS) instead of acyclovir, and the incidence and duration of facial nerve paralysis was compared in the acyclovir groups and controls. RESULTS: The incidence of facial nerve paralysis was significantly lower in the group given acyclovir before the paralysis than in the controls, and the duration of facial nerve paralysis was shorter. CONCLUSIONS: Administration of acyclovir before the paralysis reduced the incidence and duration of facial nerve paralysis. Administration of acyclovir after the paralysis improved the duration of facial nerve paralysis.

Acyclovir↗
PubMed2003

Differential brain activations during intentionally simulated and subjectively experienced paralysis.

INTRODUCTION: Distinguishing conversion disorder from malingering presents a significant challenge as the diagnosis ultimately depends on the patient's subjective report and the clinician's suspicion of an intention to deceive. Using hypnosis to manipulate the intentionality of movement inhibition in the same subjects, we used positron emission tomography (PET) to determine whether failure to move during intentionally simulated and subjectively experienced paralysis is mediated by different neural structures. METHODS: Using a within-subject design, 12 normal, hypnotised subjects were tested under two paralysis conditions during the same scanning session. Half of the scans were performed with the suggestion that the left leg was paralysed (subjectively experienced paralysis condition) and half with the leg normal but with the instruction that paralysis should be feigned (intentionally simulated paralysis condition). RESULTS: Relative increases in brain activation were seen in the right orbitofrontal cortex, right cerebellum, left thalamus, and left putamen during subjectively experienced paralysis compared to intentionally simulated paralysis, although a previously reported activation of the right anterior cingulate cortex was not seen. During intentionally simulated paralysis compared to subjectively experienced paralysis relative increases in brain activation were seen in the left ventrolateral prefrontal cortex, and a number of right posterior cortical structures. CONCLUSIONS: Our results suggest that subjectively experienced paralysis has a different neural basis to intentionally simulated paralysis. These findings have theoretical and clinical implications for malingering and related attempts to unravel the neuropsychological basis for conversion hysteria.

Journal Article↗
PubMed2006

Facial nerve paralysis caused by middle ear cholesteatoma and effects of surgical intervention.

CONCLUSIONS: The clinical and surgical findings of this study indicated advanced cholesteatoma in many patients with facial paralysis. The outcome of facial paralysis was good. Poor outcomes were observed in cases with petrosal cholesteatoma and in those who underwent surgery > or = 2 months after the onset of paralysis. OBJECTIVE: To investigate clinical features of cholesteatoma associated with facial paralysis. MATERIAL AND METHODS: Sixteen patients with facial paralysis due to middle ear cholesteatoma were reviewed. After removal of the cholesteatoma lesion, a limited area of the fallopian canal, that in which facial nerve edema or redness was evident, was opened. Incision of the epineural sheath for nerve decompression was not performed. RESULTS: Initial paralysis was incomplete in 11 patients (69%). The onset of paralysis was sudden in 12 patients (75%). Labyrinthine fistulae (n = 9; 56%) and bone destruction in the cranial fossa (n = 10; 63%) were frequently observed. Six patients (38%) were totally deaf due to labyrinthitis. The outcome of facial paralysis was good in 13 patients (81%). Patients who underwent surgery > or = 2 months after the onset of paralysis frequently had a poor outcome. Paralysis was not improved in two cases with petrosal cholesteatoma.

Adult↗
PubMed2002

Facial nerve paralysis due to chronic otitis media.

OBJECTIVE: To present the characteristics of facial paralysis caused by chronic otitis media. The role of cholesteatoma, bony dehiscence, the duration of the disease, and the results of surgical therapy in facial paralysis were reviewed. STUDY DESIGN: Retrospective case review. SETTING: Tertiary care referral center. PATIENTS: A total of 24 patients (6 women, 18 men; age range, 17-74 yr) with facial paralysis were included in the study. INTERVENTION: Canal wall down mastoidectomy was performed in 14 patients (58.3%), modified radical mastoidectomy was performed in seven patients (25%), and intact canal wall mastoidectomy was performed in three patients (16.7%). All patients had decompression of the fallopian canal from the geniculate ganglion to the stylomastoid foramen without opening the epineural sheath. RESULTS: Eighteen patients (75%) had gradual onset of facial paralysis. The most common associated symptom with facial paralysis was vertigo in six patients. Twelve patients (50%) had no associated symptoms. Facial paralysis was the sole complication in 21 patients (87.9%). Three patients had multiple complications. Labyrinthitis was the most common associated complication. Facial paralysis was associated with congenital cholesteatoma in one patient. Fourteen patients (58.3%) demonstrated dramatic recovery within 3 months after surgery. Intraoperatively, cholesteatomas were found in 17 of the patients (70.8%). The fallopian canal was intact in four patients (none of them had a cholesteatoma), and 20 patients had bone destruction or dehiscence (three patients had no cholesteatoma). The tympanic segment was the most common site of involvement in 14 patients (58.3%). CONCLUSION: A middle ear cholesteatoma was present in the majority of patients with facial paralysis caused by chronic otitis media. Gradual onset of facial paralysis was the most frequent pattern. Facial paralysis presented poor prognosis regardless of the presence of a cholesteatoma. There was no statistical difference among the results of surgical techniques.

Adolescent↗
PubMed2006

Investigation of motor dominant C5 paralysis after laminoplasty from the results of evoked spinal cord responses.

BACKGROUND: Postoperative motor dominant C5 paralysis was known as one of several complications after laminoplasty. Several theories have been proposed for postoperative segmental paralysis after laminoplasty, but its etiology remains unclear. OBJECTIVE: To investigate the possible mechanism for postoperative motor dominant C5 paralysis from intraoperative electrophysiological studies using evoked spinal cord potentials (ESCPs). METHODS: A total of 66 patients who had undergone laminoplasty due to compressive cervical myelopathy were studied retrospectively. In all patients, the symptomatic intervertebral levels of cervical myelopathy were identified by several types of the ESCPs. Motor dominant C5 paralysis was determined as at least 1 level down compared with pre-operative shoulder abduction according to the manual muscle testing. RESULTS: Five patients (7.6%) showed postoperative motor dominant C5 paralysis. C5 paralysis occurred from 1 to 3 days after surgery and compromised unilaterally in all 5 patients. The causes of cervical myelopathy were cervical spondylosis in 3 patients and ossification of the posterior longitudinal ligament in 2 patients. One patient with severe impairment (2 in manual muscle-testing [MMT] scale) did not show clinical recovery. The other 4 patients recovered to 4 or 5 on the MMT score from 3 to 6 months after the onset. Based on the findings of ESCPs, the C4-5 level was affected by cervical myelopathy in all 5 patients with postoperative motor dominant C5 paralysis (C4-5 level in 3 patients, both C4-5 and C5-6 levels in 2 patients). A high signal intensity area on T2-weighted magnetic resonance imaging (MRI) was observed in all patients who showed apparent motor dominant C5 paralysis in this study. CONCLUSIONS: Cervical myelopathy at the C4-5 level is a potential risk for motor dominant C5 paralysis. Although it is merely a speculation, when C5 radiculopathy occurs after laminoplasty, C5 paralysis becomes clinically apparent because the deltoid muscle gets predominantly innervated by C5 root due to intramedullary spinal cord damage on the C6 segment in C4-5 myelopathy before surgery. It may represent the high signal intensity area on T2-weighted MRI at the C4-5 level.

Aged↗
PubMed2006

Diagnostic testing for vocal fold paralysis: survey of practice and evidence-based medicine review.

OBJECTIVES/HYPOTHESIS: Vocal fold paralysis continues to be a dominant topic in laryngology. Although the majority of cases can be attributed to a known etiology, a significant number of patients present without a clear precipitating event. Over 1,500 studies regarding vocal fold paralysis exist in the medical literature, although only a small percentage report on the use of serum or radiographic testing for the evaluation of idiopathic paralysis. Despite this, patients are routinely subjected to diagnostic evaluation to investigate the underlying cause. To characterize contemporary practice, a national survey of the American Broncho-Esophagological Association (ABEA) membership was undertaken. It is hypothesized that the current practice of diagnostic testing for idiopathic vocal fold paralysis is not well supported by an evidence-based medicine (EBM) review of the available medical literature. STUDY DESIGN: The authors conducted a national survey, systematic EBM review of existing literature. METHODS: Surveys were mailed to all active ABEA members; responses regarding practice specialization as well as serum/radiographic diagnostic preferences for idiopathic vocal fold paralysis were tabulated and subjected to statistical analysis. To compare contemporary practice with evidence in the available literature, an EBM review was first performed. Articles for evaluation were selected from a Medline search of English-language abstracts related to adult vocal fold paralysis. The publications were individually reviewed and an EBM level and grade were assigned and compared with the survey results. RESULTS: Eighty-four of 249 active members responded with 76 (31%) replies submitted for analysis. Specific serum tests were advocated by 41 of 76 (54%) respondents, although the majority (52 of 65 [80%]) felt that they were only "occasionally" or "never" necessary. The most common tests were rheumatoid factor (38%), Lyme titer (36%), erythrocyte sedimentation rate (34%), and antinuclear antibody (33%). Fifty-one of 71(72%) felt that computed tomography (CT) was "always" or "often" necessary and 50 of 72 (69%) replied that chest radiography (CXR) was "always" or "often" necessary. There was no significant difference between CT and CXR ordering (P < .51). In contrast, magnetic resonance imaging (MRI) was described as "always" or "often" necessary in 28 of 71 (39%) of the surveys, significantly less than CT (P < .0001). There was no statistical impact of practice specialization on ordering of serum tests (P = .25) or imaging (P = .50 for CT; P = .46 for CXR; P = .45 for MRI). Following analysis of 1,510 vocal fold paralysis abstracts, 19 publications were found to be appropriate for an EBM review of serum testing with 15 available for review of radiographic imaging. Only one study presented level III evidence; the remainder were levels IV and V comprised of retrospective series and case reports. The evidence supporting serum or radiographic testing toward the evaluation of idiopathic vocal fold paralysis is given an overall grade of "C." CONCLUSIONS: Serum and radiographic testing for the evaluation of vocal fold paralysis is supported by grade "C" evidence only. There are no existing prospective studies estimating the clinical impact of testing on diagnosis or patient outcome. Current practice, as estimated by a survey of the ABEA membership, is not well founded for serum testing and only by retrospective case series with regard to imaging. Further study into the nature of idiopathic vocal fold paralysis and outcomes assessment of diagnostic paradigms may improve clinical practice.

Adult↗
PubMed1993

Rheumatoid arthritis of the cervical spine. A long-term analysis with predictors of paralysis and recovery.

We analyzed the cases of seventy-three patients who were managed over a twenty-year period for rheumatoid involvement of the cervical spine and were followed for a minimum of two years, with an average follow-up of seven years. A neurological deficit did not develop in thirty-one patients (Ranawat et al. Class I) and paralysis developed in the remaining forty-two patients: Class II in eleven and Class III in thirty-one. Of the forty-two patients in whom paralysis developed, thirty-five had operative stabilization. Seven patients were managed with a soft cervical collar because they refused or were medically unable to have the operation; all of the had an increase in the severity of the paralysis. The posterior atlanto-odontoid interval and the diameter of the subaxial sagittal canal measured on the cervical radiographs demonstrated statistically significant correlations with the presence and severity of paralysis. All of the patients who had a Class-III neurological deficit had a posterior atlanto-odontoid interval or diameter of the subaxial canal that was less than fourteen millimeters. In contrast, the anterior atlanto-odontoid interval, which has traditionally been reported, did not correlate with paralysis. The prognosis for neurological recovery following the operation was not affected by the duration of the paralysis but was influenced by the severity of the paralysis at the time of the operation. The most important predictor of the potential for neurological recovery after the operation was the preoperative posterior atlanto-odontoid interval. In patients who had paralysis due to atlanto-axial subluxation, no recovery occurred if the posterior atlanto-odontoid interval was less than ten millimeters, whereas recovery of at least one neurological class always occurred when the posterior atlanto-odontoid interval was at least ten millimeters. If basilar invagination was superimposed, clinically important neurological recovery occurred only when the posterior atlanto-odontoid interval was at least thirteen millimeters. All patients who had paralysis and a posterior atlanto-odontoid interval or diameter of the subaxial canal of fourteen millimeters had complete motor recovery after the operation. In this series, although only patients who had a neurological deficit were operated on, we observed the range of the posterior atlanto-odontoid interval that was associated with poor or no recovery after the operation, and we identified the safe range on the basis of the patients in whom paralysis did not develop.(ABSTRACT TRUNCATED AT 400 WORDS)

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