1/109. Atypical brachial plexopathy with pseudotumor cerebri. A 24-year-old woman with previously known pseudotumor cerebri syndrome (PTCS) presented with severe pain in the neck and shoulders followed by the classical symptoms and signs of bilateral brachial neuritis. At the same time, there was a recurrence of the PTCS which had been in remission for more than one-and-a-half years. Despite treatment with high doses of methylprednisolone, intravenous immunoglobulins and repeated cerebrospinal fluid drainage, both brachial plexopathy and the PTCS continued to worsen. Both lumbosacral plexuses became involved and the visual acuity deteriorated to a level such that a lumboperitoneal shunt had to be inserted. The neurological condition started to improve progressively after 8 weeks. This case is, to our knowledge, the first where brachial plexopathy has been described in association with a PTCS. Although the pathogenesis of this association is not clear, there are enough data to suggest the existence of a continuum between extended brachial plexopathy and Guillain Barre syndrome, with which PTCS has been associated in some instances. ( info) |
2/109. Management of obstetric brachial plexus palsy. OBPP is a disease with deleterious medical, psychological, and socioeconomic sequelae for the patient and his or her family. The majority of patients show acceptable spontaneous recovery with nonoperative management, which includes aggressive physical rehabilitation and electrical stimulation. There are patients with guarded prognosis, however, who have no chance of recovery unless they undergo early aggressive surgical reconstruction of the injured brachial plexus. It is of great importance to diagnose the injury type as early as possible, especially if there is minimal recovery in the early weeks of follow-up. This allows timely reconstruction to take place, earlier than 3 months for global palsy cases and at 3 months in Erb's type lesions, for best functional results. ( info) |
| We report the clinical and electrodiagnostic findings of a 39-year-old patient who presented with severe, bilateral and asymmetrical, axon-loss brachial plexopathies occurring in the midst of diabetic ketoacidosis. This patient's unusual presentation is not consistent with the rare diabetic polyradiculopathy of the upper extremities usually occurring in association with diabetic amyotrophy. ( info) |
4/109. Chronic demyelinating hypertrophic brachial plexus neuropathy. A patient with unilateral, painless, chronic progressive upper limb sensorimotor deficit showed electrophysiological evidence of a focal demyelinating neuropathy with almost complete conduction block across the brachial plexus. magnetic resonance imaging disclosed marked brachial plexus hypertrophy. Intravenous immunoglobulin led to fast and complete recovery, maintained by intermittent perfusions. Hypertrophic brachial plexus neuropathy can be a presentation of focal chronic inflammatory demyelinating polyradiculoneuropathy. Objective and quantitative assessment of hand function is useful to evaluate treatment results and to optimize treatment regimens. ( info) |
5/109. Delayed brachial plexus neurapraxia complicating malunion of the clavicle. Delayed brachial plexus neurapraxia is a rare complication of midshaft clavicular fracture. The symptoms are variable and occur insidiously. Surgical decompression to release the compression of brachial plexus is the treatment of choice and usually has a good result. We report a patient whose brachial plexus was compressed by malunion of the clavicle. This patient had a good outcome after treatment with intramedullary nailing and Knowles pin fixation after corrective osteotomy without bone grafting. ( info) |
6/109. Neoplasm as a cause of brachial plexus palsy in neonates. Two patients with neonatal onset of arm weakness resulting from neoplastic involvement of the brachial plexus who were initially considered to have obstetric brachial plexus palsies are reported. The first patient was a 7-day-old female who presented with a left supraclavicular mass that was first detected at 2 days of age and left proximal arm weakness. The weakness involved the whole arm within 3 days. The mass was a malignant rhabdoid tumor. The second patient was a 28-month-old male who presented with slowly progressive right arm weakness, which began at 3 weeks of age, and episodes of scratch marks on the arm that began at 4 months of age. magnetic resonance imaging revealed a plexiform neurofibroma of the brachial plexus. The features that are suggestive of a brachial plexus palsy caused by a neoplasm rather than of obstetric brachial plexus palsy include the following: the onset of weakness after the first day of age, with a progressive course; a history of a normal delivery and birth weight; the absence of signs of a traumatic injury or injuries; the appearance before 7 days of age of a growing supraclavicular mass without radiographic evidence of a clavicular fracture; and recurrent scratch marks on the weak arm. ( info) |
| BACKGROUND: Shoulder hemorrhage resulting in brachial plexus neuropathy is a rare occurrence most often seen in cases of traumatic injury or anticoagulation therapy. We report a unique case of spontaneous brachial plexus hemorrhage. CASE DESCRIPTION: This is the first report of a spontaneous shoulder hemorrhage in which a 48-year-old jackhammer operator presented to the emergency department with a sudden onset of right shoulder pain and upper extremity pain and numbness. Imaging studies revealed a hematoma in the right axilla and chest wall. Without evidence of active bleeding or worsening neurologic deficit, this patient was treated conservatively with pain control and observation and eventually experienced a full recovery. Had there been persistent neurologic deficit, however, surgical evacuation would have been indicated. CONCLUSIONS: Cases of nerve compression caused by a hematoma should be analyzed on the basis of the severity of the neurologic deficit and not on the underlying cause of bleeding. Conservative treatment may be indicated in cases of mild or improving neurologic deficit, but regardless of its etiology, a hematoma that results in severe or worsening neurologic symptoms must be surgically evacuated to prevent permanent nerve damage. ( info) |
| BACKGROUND AND OBJECTIVES: This report illustrates that brachial plexus palsy can result from either interscalene block or total shoulder arthroplasty. It is often impossible to determine which procedure caused the deficit; therefore, we believe the focus should be placed on treatment of the neurologic deficit. This report provides a suggested algorithm for diagnosis and treatment of postprocedure brachial plexus palsy. methods: Interscalene block was used as the operative anesthetic for our patient's total shoulder arthroplasty. Complete brachial plexus palsy was diagnosed postoperatively. RESULTS: The patient's postoperative treatment and recovery are described. CONCLUSIONS: Proper diagnosis and treatment of postprocedure brachial plexus palsy may improve recovery of function. Several precautions may reduce the likelihood of brachial plexus palsy following interscalene block for total shoulder arthroplasty. ( info) |
9/109. Retraining of a competitive master athlete following traumatic injury: a case study. PURPOSE: The purpose of this study was to examine the physiological effects of detraining and retraining in a female master cyclist (age, 49.5 yr; wt, 54 kg) following a surgically-treated clavicular fracture complicated by brachial plexus impingement. methods: Variables associated with cycling performance, including VO2max, lactate threshold (LT), power output at a blood lactate concentration of 4 mM (LT(4 mM)), peak power output (PPO), muscular resistance to fatigue measured by a timed ride to exhaustion at 110% of peak power output (PPO110), and body composition (hydrostatic weight) were assessed 2 d before the injury when the subject was at the peak of her competitive season, and at days 0, 14, 28, 42, and 77 of the retraining period. Retraining gradually increased from 3 h x wk(-1) to 9-10 h x wk(-1) with an increase in intensity from approximately 70 to 95 % of HRmax. RESULTS: Detraining resulted in a 25.7% decrease in VO2max and a 16.7% and 18.9% decrease in LT and LT(4 mM), respectively, while peak power output and PPO110 declined 18.2% and 16.6%, respectively. Body fat percent increased 2.1 percentage points, while fat-free mass decreased nearly 2 kg. After 2 wk of retraining, all variables except the LT and LT(4 mM) had improved considerably; however, VO2max was still 14.8% lower and PPO and PPO110 were 12.7% and 5.7% lower than preinjury values. By the 11th week of retraining, all variables had essentially returned to their preinjury values. CONCLUSION: These data demonstrate a pattern of retraining in which aerobic power steadily improved over 6 wk, while measures of lactate threshold did not change until the fourth week of retraining when the intensity of training was markedly increased. Additional data are needed to determine whether this pattern of retraining would be consistent in other master athletes. ( info) |
10/109. Brachial plexopathy associated with diffuse edematous scleroderma. peripheral nervous system (PNS) involvement is rare in systemic sclerosis (SSc), usually restricted to peripheral nerve entrapment. To our knowledge, only one case of scleroderma with brachial plexus involvement has been reported previously. We report here on a 61-year-old woman with past history of limited cutaneous SSc who developed motor deficiency in the left arm concomitant with diffuse edematous scleroderma without evidence for trauma or compression of the brachial plexus. After six months intravenous pulse cyclophosphamide therapy, dramatic improvement of skin and neurological involvement was observed. ( info) |