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Spinal or Segmental Myoclonus
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(See also page 1066) The notion that monophasic restricted myoclonus always emanates from the cerebral cortex, cerebellum, or brainstem cannot be sustained, for there are forms that are traceable to a purely spinal lesion A subacute spinal myoclonus of obscure origin was described many years ago by Campbell and Garland, and similar cases continue to be cited in the literature We have seen several such cases where myoclonus was isolated to the musculature of the abdominal or thoracic wall on one side or to the legs; only rarely were we able to establish a cause, and the spinal uid has been normal It takes the form of an almost continuous arrhythmic jerking of a group of muscles This form has been referred to as propriospinal, particularly when it involves repetitive exion or extension myoclonus of the torso that is aggravated by stretching or action A sharply demarcated segmental myoclonus has been induced in animals by the Newcastle disease virus, and examples of myelitis with irregular segmental myoclonic jerks (either rhythmic or arrhythmic) have been reported in humans Many such cases involve the legs or a few muscles of one leg In our experience, this type of myelitic myoclonus has occurred following zoster myelitis, postinfectious transverse myelitis, and rarely with multiple sclerosis, epidural compression, or after spinal traumatic injury A paraneoplastic form has also been described When highly ionic contrast media were used for myelography, painful spasms and myoclonus sometimes occurred in segments where the dye was concentrated by a block Treatment is dif cult, and one resorts to a combination of anticonvulsants and diazepines, just as in cerebral myoclonus The glycine inhibitor levetiracetam has reportedly been successful when other drugs have failed (Keswani et al)
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Pathophysiology of Myoclonus Multiplex
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It seems logical to assume that myoclonus is caused by abnormal discharges of aggregates of motor neurons or interneurons because of the directly enhanced excitability of these cells or the removal of some inhibitory mechanism Sensory relationships are a prominent feature of myoclonus multiplex, particularly those related to metabolic disorders, and will eventually shed some light on the mechanism Flickering light, a loud sound, or an unexpected tactile stimulus to some part of the body initiates a jerk so quickly and consistently that it must utilize a direct sensorimotor pathway or the mechanism involved in the startle reaction Repeated stimuli may recruit a series of incremental myoclonic jerks that culminate in a generalized convulsion, as often happens in the familial myoclonic syndrome of UnverrichtLundborg Another type of sensory myoclonus is the audiogenic form, characteristic of Tay-Sachs disease Each auditory stimulus results in blinking, abrupt elevation of the arms, and other movements This generalized myoclonic jerk does not fatigue with successive stimuli and is modality-speci c
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CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE
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Evidence implicating cortical hyperexcitability in myoclonus is indirect, being based mainly on the nding that the cortical components of the somatosensory evoked potential are exceedingly large In some such instances, the myoclonic jerks also have a strict time relationship ( time-locked ) to preceding spikes in the contralateral rolandic area, indicating that the cerebral cortex may play an active and perhaps primary role in the elaboration of myoclonus (Marsden et al; Brown et al); however, it is just as likely that these cortical potentials are projected from subcortical structures that also project to descending motor pathways In humans, the indication is that postanoxic action myoclonus has its basis in re ex hyperactivity of the reticular formation and that the only consistent damage is in the cerebellum rather than in the cerebral cortex (see above, under Intention or Action Myoclonus ) Also as already noted, several types of myoclonus are closely coupled with cerebellar cortical degenerations Pathologic examinations have been of little help in determining the essential sites of this unstable neuronal discharge because, in most cases, the neuronal disease is so diffuse The most restricted lesions associated with myoclonus are seemingly located in the cerebellar cortex, dentate nuclei, and pretectal region A lack of modulating in uence of the cerebellum on the thalamocortical system of neurons has been postulated as a likely mechanism, but it is uncertain whether the disinhibited motor activity is then expressed through corticospinal or reticulospinal pathways For example, pentylenetetrazol (Metrazol) injections evoke myoclonus in the limbs of animals, and the myoclonus persists after transection of corticospinal and other descending tracts until the lower brainstem (medullary reticular) structures are destroyed
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