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At least 19 recordsLinked to original sources
PubMed1991

Brachial plexus neuropathy.

Brachial plexus neuropathy is a common syndrome that, although a distinct clinical entity, is often unrecognized. The illness is characterized by the acute onset of shoulder girdle pain without constitutional symptoms. The pain persists for 1 to 2 weeks, then subsides, with the development of weakness and atrophy in the affected muscles. Good recovery usually occurs but may take up to three years. There is no effective treatment. Since this condition may masquerade as bursitis, cervical disc disease, or other conditions commonly seen by general physicians, it is important to recognize this disorder.

Adult↗
PubMed2005

Friday night palsy: an unusual case of brachial plexus neuropathy.

Brachial plexopathy can result from traction injury, radiation injury, local or metastatic cancer, hereditary, or idiopathic causes. However, brachial plexopathy resulting from malposition of an arm during sleep, similar to Saturday night palsy, has not been reported. We report a case of brachial plexus neuropathy that occurred after the patient slept on his shoulder and arm following excessive alcohol consumption on a Friday night.

Adult↗
PubMed1980

Brachial plexus neuropathy. Three cases in children.

Brachial plexus neuropathy is an acute neurologic disorder characterized by pain, weakness, and atrophy of the muscle groups affected. Although well documented in the adult literature, relatively few cases have been reported in children. Despite the lack of knowledge concerning its etiology, and lack of an effective therapy, the long-term prognosis is excellent. It is perhaps for these reasons that spinal fluid analysis is not routinely performed during the acute phase of this illness. An evaluation of the clinical course of three children, together with epidemiologic data, suggests that early lumbar punctures and an extensive search for an infecting viral agent, notably coxsackievirus B, are warranted.

Brachial Plexus↗
PubMed1997

Chronic relapsing brachial plexus neuropathy with persistent conduction block.

Idiopathic brachial plexus neuropathy (BPN) is an immune-mediated disorder characterized by an acute onset of painful weakness in one or both upper extremities. The course is usually monophasic with gradual improvement over months; however, occasionally BPN can recur. Electrophysiologic studies suggest the pathogenesis is primarily axonal in the majority of cases. We describe an unusual case of BPN in which the patient had a chronic and relapsing course of painless weakness associated with conduction blocks and other electrophysiologic features of demyelination across the brachial plexus. The patient improved following treatment with intravenous immunoglobulin. The neuropathy falls within the spectrum of chronic inflammatory demyelinating polyneuropathy and multifocal motor neuropathy.

Action Potentials↗
PubMed1978

Carcinomatous versus radiation-induced brachial plexus neuropathy in breast cancer.

A retrospective study was performed of 18 women in whom ipsilateral brachial plexus neuropathy developed after treatment for carcinoma of the breast. In the absence of metastatic tumor elsewhere, the only distinguishing feature between carcinomatous neuropathy and radiation-induced neuropathy was the symptom-free interval after mastectomy and radiation therapy. Women with an interval of less than a year have radiation-induced neuropathy. Brachial plexus exploration in difficult diagnostic situations will permit early treatment and avoid debilitating loss of function. Brachial plexus exploration for biopsy is safe and free of complications if performed carefully. Treatment of carcinomatous neuropathy is most likely to succeed if the tumor is hormonally sensitive, but radiotherapy may also be effective. Treatment of radiation-induced neuropathy remains largely ineffective.

Adenocarcinoma↗
PubMed1995

Postoperative brachial plexus neuropathy after total knee replacement under spinal anaesthesia.

We describe a case of idiopathic postoperative brachial plexus neuropathy. A 68-yr-old man underwent elective total knee replacement under spinal anaesthesia. Two days after surgery, there was sensory loss and weakness in the right forearm and hand, which suggested an ulnar nerve neuropathy. Two weeks later the patient complained of a dull ache between the scapulae, followed by a burning sensation in the forearm and severe pain in the elbow. A diagnosis of brachial plexus neuropathy was made based on clinical examination and nerve conduction studies. The pain disappeared after a few months, although weakness of the right arm persisted 9 months later. The differential diagnosis between brachial plexus neuropathy and ulnar nerve neuropathy is important, as the prognosis of brachial plexus neuropathy is generally good.

Aged↗
PubMed1985

Brachial plexus neuropathy following high-dose cytarabine in acute monoblastic leukemia.

We describe brachial plexus neuropathy with high-dose cytarabine (Ara-C) therapy in a man who had acute monoblastic leukemia. Signs and symptoms of brachial plexus neuropathy appeared on two occasions within hours of exposure to high-dose Ara-C. Central nervous system complications have been described following systemic and intrathecal Ara-C. High-dose Ara-C has not been implicated previously as a cause of brachial plexus neuropathy.

Arm↗
PubMed1998

Acquired brachial-plexus neuropathy in the neonate: a rare presentation of late-onset group-B streptococcal osteomyelitis.

Acquired brachial-plexus neuropathy outside the immediate neonatal period is uncommon. Pseudopalsy of a limb, associated with osteomyelitis, is well recognized. Acquired brachial-plexus neuropathy as the initial presentation of osteomyelitis of the humerus in the neonatal period is described. Three infants presented at 3, 15, and 21 days respectively, with acute monoplegia consistent with brachial-plexus neuropathy. The infants were afebrile and generally well. Initial radiographs of the humerus were normal and blood cultures grew group-B streptococcus in all infants. Nerve conduction studies were consistent with brachial-plexus neuropathy. Following intravenous antibiotics, there was complete recovery in all infants. Osteomyelitis of the humerus should be considered in infants in whom there are no overt signs of sepsis and who present with brachial-plexus neuropathy. Early diagnosis and appropriate treatment should result in a complete neurological recovery.

Brachial Plexus↗
PubMed1995

Hereditary neuropathy with liability to pressure palsies and inherited brachial plexus neuropathy--two genetically distinct disorders.

OBJECTIVE: To determine whether hereditary neuropathy with liability to pressure palsies (HNPP) and inherited brachial plexus neuropathy (IBPN) are genetically distinct disorders and to evaluate the usefulness of fluorescence in situ hybridization (FISH) for diagnosing HNPP in individual patients. DESIGN: We studied representative metaphases from patients with HNPP and IBPN with use of FISH and a DNA probe. MATERIAL AND METHODS: With use of FISH, 14 persons from 4 unrelated families with HNPP and 7 members from 3 unrelated families with IBPN were studied. We used a DNA probe that hybridizes to chromosome 17p11.2 in an area thought to be deleted in HNPP. RESULTS: Each participant in this study who had HNPP showed deletion of this chromosome site. Each of the 10 control subjects and 7 patients with IBPN showed normal fluorescent signals on both number 17 chromosomes. CONCLUSION: These results demonstrate that HNPP and IBPN are genetically different. FISH with this probe is a sensitive and specific method for detecting the chromosomal deletion in individual patients without the use of family studies or linkage analysis.

Brachial Plexus Neuritis↗
PubMed1995

[Hemidiaphragmatic paralysis as a manifestation of familial brachial plexus neuropathy].

We present a patient with familial brachial plexus neuropathy (FBPN) who is in the second generation of a family found to have this disease. The patient suffered phrenic paralysis, which has only been previously described in association with FBPN in 4 similar cases, all of which also involved the left phrenic nerve. The side of phrenic paralysis's was unrelated to the side where brachial plexus lesions occurred. We believe that paralysis of the diaphragm, although rare, can be considered a sign of FBPN and that therefore this disease should be included in the differential diagnosis of such paralysis. This is particularly so whenever family or personal history suggest that the peripheral nervous system may be involved, compromising the brachial plexus, or whenever facial or digital dysmorphia is present.

Adult↗
PubMed1985

Brachial plexus neuropathy in the population of Rochester, Minnesota, 1970-1981.

Brachial plexus neuropathy (BPN) is a clinical entity of unknown cause characterized by the acute or subacute onset of pain and weakness, with occasional atrophy of the arm muscles. Information on the incidence of the disease in a delineated population is lacking, as the data available on BPN have come essentially from case reports or selected series. Using the Mayo Clinic records-linkage system as the source of data, 579 clinical records were reviewed of Rochester, Minnesota, residents in which a diagnosis suggestive of BPN was reported for the period 1970 through 1981. Eleven cases fulfilled all criteria, providing an overall annual incidence rate of 1.64 cases per 100,000 population. An infectious disease and/or tetanus toxoid immunization preceded the onset of BPN in 4 cases. The upper brachial plexus was involved in 6 cases, the lower brachial plexus in 2, and the whole plexus in 3; in 1 case there was bilateral BPN. The neuropathy ran a mild to moderate course in 10 cases, and complete recovery was recorded in 6, with slight residua in the others. The occurrence of antecedent events and the features of the disease are supportive of the concept of an immune-mediated process.

Adult↗
PubMed1993

Anti-peripheral nerve myelin antibodies and terminal activation products of complement in serum of patients with acute brachial plexus neuropathy.

OBJECTIVE: To determine if complement-fixing antibodies to peripheral nerve myelin (anti-PNM antibodies) and terminal complement activation products were increased in serum of patients with brachial plexus neuropathy compared with normal controls. DESIGN: Case series. SETTING: University medical center. PATIENTS: Three patients (aged 6, 39, and 51 years) with acute brachial plexus neuropathy were studied during the acute and recovery phase of their disease. METHODS: Anti-PNM antibodies were measured in serum samples obtained from three patients and 25 normal controls with the C1 fixation and transfer assay. Soluble terminal complement activation products, SC5b-9, were measured by enzyme-linked immunosorbent assay (ELISA) in serum samples of one patient with brachial plexus neuropathy and of five normal controls. RESULTS: Both serum anti-PNM antibodies and soluble terminal complement activation products were increased in the acute phase of brachial plexus neuropathy compared with normal control values and decreased several months later during clinical recovery. CONCLUSION: Complement dependent, antibody-mediated demyelination may participate in the peripheral nerve damage of brachial plexus neuropathy.

Acute Disease↗
PubMed1975

Recurrent brachial plexus neuropathy.

The clinical, electrophysiological and pathological changes in 3 patients with recurrent attacks of non-traumatic brachial plexus neuropathy have been described. Two had recurrent attacks and a dominant family history of similar attacks, together with evidence of lesser degrees of nerve involvement outside the brachial plexus. In one patient the attacks were moderately painful, while in the other there was little or no pain. Only one showed undue slowing of motor nerve conduction during ischaemia, but in both cases the sural nerves had the changes of tomaculous neuropathy, with many sausage-shaped swellings of the myelin sheaths, and extensive segmental demyelination and remyelination. The third patient had two attacks of acute brachial plexus neuropathy which were both extremely painful. The clinical features were compatible with a diagnosis of neuralgic amuotrophy. In the second attack, there was vagus nerve involvement and the sural nerve showed evidence of healed extensive segmental demyelination. The various syndromes presenting with acute non-traumatic brachial plexus neuropathy are reviewed, and a tentative nonsological classification advanced. Most patients fall into the category of acute, painful paralysis with amyotrophy, with no family history and no evidence of lesions outside the brachial plexus. It is suggested that the term "neuralgic amyotrophy" be restricted to this group. Patients with features outside this clinical picture probably suffer from other disease entities presenting with brachial plexus neuropathy. The familial cases constitute one or more aetioliogical subgroups, differing from neuralgic amyotrophy in the frequency of recurrences, the relative freedom from pain in the attacks, the frequency of nerve lesions outside the brachial plexus, and of hypotelorism. Individual attacks of acute brachial plexus neuropathy, however, may be identical in patients with the different diseases, and further pathological and biochemical studies are awaited to aid in nosology.

Acute Disease↗
PubMed1990

Recurrent brachial plexus neuropathy and giant cell arteritis.

A 73-year-old women presented with a recurrent form of sporadic brachial plexus neuropathy, the so-called Parsonage and Turner syndrome. This diagnosis is based on clinical and electromyographic findings. Interestingly a biopsy of the temporal artery demonstrated a giant cell arteritis. The clinical picture started 2 weeks after an upper respiratory tract illness. The possible viral etiology of giant cell arteritis is considered. We think an immunological rather than ischemic disturbance may have caused the recurrent brachial plexus neuropathy. This case report suggests that giant cell arteritis be considered in the investigation of the Parsonage and Turner syndrome.

Aged↗
PubMed2001

Arteritis and brachial plexus neuropathy as delayed complications of radiation therapy.

Radiation-induced arteritis of large vessels and brachial plexus neuropathy are uncommon delayed complications of local radiation therapy. We describe a 66-year-old woman with right arm discomfort, weakness, and acrocyanosis that developed 21 years after local radiation for breast adenocarcinoma. Arteriography revealed arteritis, with ulcerated plaque formation at the subclavian-axillary artery junction, consistent with radiation-induced disease, and diffuse irregularity of the axillary artery. Electromyography showed a chronic brachial plexopathy. The patient's acrocyanosis, thought to be due to digital embolization from her vascular disease, improved with antiplatelet therapy. The concurrent combination of radiation-induced arteritis and brachial plexopathy is uncommon but should be considered in patients presenting with upper extremity pain or weakness after radiation therapy.

Adenocarcinoma↗
PubMed2000

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.

Adult↗