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Dr Bereitschaft.

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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.
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