Less than 1% of patients with spinal cord compression have ataxia as the first symptom, and less than 7% of all patients with malignant spinal cord compression exhibit ataxia on the initial examination [I, 3 , 51. Gilbert and associates [l) described 7 patients with gait ataxia “. . . as the most striking sign on examination,” but apparently only one of their patients had truncal ataxia as the sole initial finding. As noted by Gilman and &sociates 121,the specific finding of truncal ataxia but no appendicular ataxia most often indicates disease of the midline cerebellar structures, or less commonly disease of the cerebellar hemisphere. They reported the highest incidence of pure truncal ataxia in patients with midline lesions, less often in those with right cerebellar hemisphere involvement, and least often in those with involvement of the left cerebellar hemisphere. In our patient, complete block of contrast material without radiographic evidence of changes in the midline of the cerebellum s u g e e ~ sthat the basis for the truncal ataxia may have been dysfu.,ction of the ascending spinoccrebellar pathways within the spinal cord. Dorsolateral white matter ischemia caused by spinal cord compression could result in impaired conduction of the ascending dorsal spinocerebellar tract m d subsequeht mismatched vermal integration of ventral spinocerebellar tract information (copy of efferent central instruction) and dorsal spinocerebellar tract information (afferent truncal feedback). This imbalance may then result in truncal ataxia. This cannot be said with complete certainty, since specific pathological evidence of involvement of spinocerebellar pathway(s) was not available; additionally, the complete spinal block may implicate dysfunction of multiple tracts. “Department of Neurology ?Department of Neuroradiology Mount Sinai School of Medicine I Gustaue Levy Place New York, NY I0029 References 1. Gilbert RW, Kim J-H, Posner JB: Epidural spinal cord compression from metastatic tumor: diagnosis and treatment. Ann Neurol 3:40-51, 1978 2. Gilman S, Bloedel JR, Lechtenberg R: Disorders of the Cerebellum. Philadelphia, Davis, 1981, pp 194-198 3. Greenberg HS, Kim J-H, Posner JB: Epidural spinal cord compression from metastatic tumor: results with a new treatment protocol. Anh Neurol 8:361-366, 1980 4. Henson RA, Urich H: Cancer and the Nervous System. Boston, Blackwell, 1982, pp 120-155; 346-368 5. Rodriguez M, Dinapoli RP: Spinal cord compression with special reference to metastatic epidural tumors. Mayo Clin Proc 55:442448, 1980 Dr Bereitschaft? K G. Woodward, M D In a recent study of cortical potentials related to movements published in the Annals [2}, the authors referred to “Bereitschaft’s potential,” which implies that it might have been 512 Annals of Neurology Vol 2 1 N o 5 May 1987 described by one Bereitschaft. I believe this comes from a mistranslation, as Bereitschaft means readiness. The correct term is Bereitschaftpott.ntia1,or readiness potential [1). Department of Neurologv Northwestern University Chicago, IL 60611 References 1. Halliday AM: Evoked brain potentials how far have we come since 1875? In Barber C (ed): Evoked Potentials. Baltimore, University Park Press, 1980, pp 3-18 2. Lee B1, Luders H, Lesser RP, et al: Cortical potentials related to voluntary and passive finger movements recorded from subdural electrodes in humans. Ann Neurol 20:32-37, 1986 Reply Hans Liiders, MD The comments of Dr Woodward are well taken. Certainly the way we spelled Bereitschaftspotential was wrong. I would also like to point out that in D r Woodward’s letter my name is misspelled. The correct spelling is Liiders with an umlaut. Department of Neurology The Clevelmd Clinic Foundation Cleveland, OH 44106 Cortical Stimulation Does Not Cause Short-Term Changes in the Electroencephalogrm Leonard0 G. Cohen, ME), and Mark Hallett, MD Recently, a technique was developed that permits transcranial stimulation of areas of the human cerebral cortex wirhout causing undue discomfort in awake persons 123.It is now possible to measure central motor conductioq velocities in normal subjects and in patients with different diseases. Moreover, it is now possible to measure the influence of a descending motor command on spinal cord function. As has been pointed out by Young and Cracco 131, this is still a research technique and mmy questions remain unanswered. One of them IS: Will cortical stimulation produce seizures or kindling of an epileptic tocus in some subjects? To help resolve this issue, we recorded the electroencephalograms (EEGs) of ten normal volui~teersbefore and after a session of cortical stimulation. These studies were done to satisfy Food and Drug Administration requirements for approval of our Investigational Device Exemption for the Digitimer Isolated Stimulator D-180 which we used for delivering stimulation. Our protocol was approved by the NINCDS Clinical Research Subpanel, and consent forms were signed by each participant.