Intravenous immunoglobulin-induced osmotic nephrosis.

Intravenous immunoglobulin preparations are being used for an increasing number of indications in clinical medicine. To minimize adverse reactions, sugar additives such as sucrose are added to some preparations to serve as stabilizing agents. We describe a patient treated with an immunoglobulin preparation containing sucrose who developed a fully reversible form of acute renal failure with histologic changes characterized by vacuolization and swelling of renal proximal tubular cells. We believe the high concentration of sucrose in the immunoglobulin preparation resulted in osmotic injury to the renal tubules. Such changes, which are identical to those described in humans and experimental animals given intravenous infusions of hypertonic sucrose, have come to be known as osmotic nephrosis. Risk factors for the development of this lesion are renal insufficiency and volume depletion. The risk for such injury can be minimized by further diluting the immunoglobulin preparation and slowing the infusion rate.

Prophylactic drug therapy in cerebrovascular disease.

Aspirin in doses of 325 mg to 1,300 mg per day is the drug of choice for prophylactic therapy in cerebrovascular disease. Ticlopidine, a platelet antagonist, is available for use in patients who cannot tolerate aspirin or who have not had success with aspirin therapy. Although ticlopidine is more effective than aspirin in preventing stroke, its use may be somewhat limited due to cost and the uncommon but serious side effect of neutropenia. Low-dose warfarin remains the drug of choice for the prevention of cardioembolic stroke. The role of warfarin in ischemic cerebrovascular disease is unknown.

Denervated human skeletal muscle: MR imaging evaluation.

Because determination of neurologic integrity after severe limb trauma is crucial in patient care, the authors assessed magnetic resonance (MR) imaging as a tool to map denervated motor units of skeletal muscle in patients with traumatic peripheral neuropathy. Denervation was confirmed in 22 patients with use of electromyography, surgery, or both. MR imaging was performed with moderately T1- and T2-weighted spin-echo and short-tau inversion-recovery (STIR) sequences. MR imaging was unreliable in depicting acute denervation. Muscles of patients with subacute denervation had prolonged T1 and T2, which contributed to conspicuous hyperintensity on STIR images. Chronically denervated muscles showed marked atrophy, variable changes on STIR images, and conspicuous fatty infiltration on T1-weighted images. Normal variants in motor unit anatomy were seen in denervated muscle volumes outside the expected distribution of the injured nerve. MR imaging is promising for the noninvasive mapping and monitoring of denervated muscle in subacute and chronic phases of peripheral neuropathy.

MRI-guided biopsy in inflammatory myopathy: initial results.

The purpose of this report is to describe our initial experience with techniques employing magnetic resonance imaging (MRI) to guide the choice of muscle to be biopsied in patients suspected of having inflammatory myopathy. Five patients with a clinical diagnosis of inflammatory myopathy (IM) were studied. Four were imaged prior to biopsy. Four had repeated examinations, either immediately following biopsy or to evaluate disease progression. Use of MRI to localize muscle lesions was associated with abnormal pathologic findings in all cases, including histopathologic demonstration of lymphocyte infiltration in three cases of idiopathic polymyositis; nonspecific myopathic changes were seen in one patient with probable dermatomyositis and in one patient with chronic inflammatory polyneuropathy and high serum creatine kinase levels (> 45,000 IU/ml). The precise location of the area sampled by biopsy was visible in only one of four postbiopsy images. MRI shows promise in identifying pathologic muscle in patients suspected of having one of the inflammatory myopathies; however, further refinement of localization techniques may be needed to optimize histopathologic diagnoses.

Management controversy. Medical versus surgical therapy for spontaneous intracerebral hemorrhage.

The controversy surrounding the management of intracranial hemorrhage seems to have been quieted by a large group of recent studies. Future efforts must focus on expansion of the current population screening projects for early detection of hypertension. Whereas some potential exists for new innovative surgical techniques to offer some benefit, it should be kept in mind that most of these patients suffer from end-stage cardiovascular, cerebrovascular, and peripheral vascular disease.

MRI evaluation of amyloid myopathy.

Amyloid myopathy is a rare complication of primary amyloidosis. The magnetic resonance imaging (MRI) features of two patients with amyloid myopathy were studied. Slight prolongation of muscle T1 and T2 relaxation times was evident but the striking abnormality was marked reticulation of the subcutaneous fat. The clinical findings of indurated extremities far exceeds the minimal signal intensity alteration seen in the muscles. The MR appearance of amyloid myopathy differs from that of other neuromuscular conditions in the minimal changes found in muscle, but the striking abnormality seen in subcutaneous fat makes it distinct from many neuromuscular conditions.

Use of amphetamine in the treatment of aphasia.

The effects of d-amphetamine on the recovery of aphasia following stroke was examined in 6 patients. Patients entered the study between 10 and 30 days post onset and were followed for 3 months. The Porch Index of Communicative Ability was used to project a 6 month recovery score. By 3 months post onset, 5 of the 6 patients obtained scores in excess of 100% of the 6 month projections.

Preliminary results of a double-blind, randomized, placebo-controlled trial of cyclosporine in myasthenia gravis.

We randomly assigned 20 patients with progressively worsening generalized myasthenia gravis of recent onset whose illness was not controlled by anticholinesterase therapy to treatment with either cyclosporine (6 mg per kilogram of body weight per day) or placebo. Patients who had been treated with thymectomy, steroids, or other immunosuppressive agents were excluded. The duration of treatment was 12 months. Disease activity was assessed by quantified strength testing and by measurements of antihuman acetylcholine-receptor antibody. Patients were assessed at 6 months and 12 months, or at the following early end points: drug failure (doubling of creatinine), treatment failure (respiratory or swallowing difficulty), or protocol violation (stopping medication for more than five days). At six months, patients in the cyclosporine group had had significantly more objective improvement in strength; one early end point had been reached (drug failure; no treatment failures). In the placebo group, three early end points had been reached (all treatment failures). The decline in titers of acetylcholine-receptor antibody was larger in the treated group, although the difference was not statistically significant. At the end of the study (after 12 months of treatment or arrival at an earlier end point), improvement in strength and reduction in titers of anti-receptor antibody continued to be greater in the cyclosporine group. Nephrotoxicity occurred in three patients receiving cyclosporine but was nonprogressive with a reduction in dosage and reversible with discontinuation of the drug. These results are preliminary and need confirmation, but we conclude that cyclosporine is probably an effective therapy in some patients with myasthenia gravis.

Facial pain of neurologic origin mimicking oral pathologic conditions: some current concepts and treatment.

A variety of pain syndromes of the face can arise from extradental pathologic conditions that can, at times, be confusing. Awareness of pain syndromes of neurologic origin that can mimic pathologic dental conditions is helpful. When doubt persists, rather than extract or endodontically treat a tooth, injection of a local anesthetic to the most sensitive areas can be a helpful diagnostic test. We recognize that there are many entities, including dental and temporomandibular joint syndromes, that much more often account for facial pain. However, we believe that those who most often treat these patients should also be aware of some of the advances in the understanding of the causes and treatment of the neurologic syndromes that can mimic pathologic oral conditions.