Neuromyotonia in a muscle flap producing a convulsing breast: successful treatment with botulinum toxin.
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Botulinum Toxins, Type A↗
Biomedical subjects
D R Wren
Publications and source records attributed to D R Wren.
Unilateral abdominal muscle herniation with pain: a distinctive variant of diabetic radiculopathy.
Thoracic diabetic radiculopathy causing truncal pain and abdominal muscle bulging is a recognized though extremely rare complication of diabetes. We report here six cases, describing their clinical features and natural history in detail: the condition affects predominantly middle-aged men, usually on the right side of the abdominal wall, involving three to five adjacent nerve roots between T6 and T12. It may be accompanied by profound weight loss which is not normally due to poorly controlled diabetes. Complete resolution of this syndrome occurs after 3 to 12 months.
Abdominal Muscles↗
Spinal rigidity following acute myelitis.
A patient with a 2(1/2)-year history of painful spasms and rigidity of both lower limbs is described. Symptoms began after an episode of acute myelitis. The spasms--which were spontaneous and stimulus sensitive and occurred on voluntary action--involved the repetitive grouped discharge of motor units. Continuous motor unit activity was present at rest in the muscles of both legs, and cutaneomuscular reflexes were abnormal. This patient is similar to those recently reported as having stiffness and spasms of the legs due to a possible chronic spinal interneuronitis and provides further evidence that this kind of movement disorder may be caused by spinal cord pathology.
Acute Disease↗
Oligodendrocytes and oligodendrocyte/type-2 astrocyte progenitor cells of adult rats are specifically susceptible to the lytic effects of complement in absence of antibody.
The central nervous system of individuals with multiple sclerosis contains lesions specifically characterized by breakdown of myelin sheaths associated with a general failure of repair of demyelinating damage. The cause of myelin breakdown is unknown. Although immune mechanisms have been implicated in this breakdown, no convincing demonstrations of specific immune reaction against myelin have yet been provided in multiple sclerosis patients. Similarly, the cellular biological mechanisms which underlie the failure of myelin repair are unknown. We have found that (i) oligodendrocytes, the cells that produce myelin sheaths in the central nervous system, and (ii) oligodendrocyte/type-2 astrocyte (O/2A) progenitor cells derived from optic nerves of adult rats bind and activate complement in the absence of antibody in vitro, leading to destruction of these cells. Susceptibility to antibody-independent lysis by complement was a cell-type-specific trait of oligodendrocytes and adult O/2A progenitors and was not shared by perinatal O/2A progenitors, type-2 astrocytes, type-1 astrocytes, meningeal cells, or Schwann cells. We suggest that the susceptibility of oligodendrocytes and adult O/2A progenitor cells to complement-induced lysis, combined with other specific properties of adult O/2A progenitors, are consistent with--and may be a contributing factor--both in the generation of demyelinating lesions in multiple sclerosis and also in the failure of these lesions to be successfully repaired in adult multiple sclerosis patients.
Aging↗