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• Authors' reply
  Tetsuro Ago
  Published on: 13 April 2016
• Making matters worse, ipsilaterally: A new explanation
  Iraj Derakhshan
  Published on: 13 April 2016

• Published on: 13 April 2016

  Authors' reply

  • Tetsuro Ago, MD, PhD
  • Other Contributors:
    • Takanari Kitazono

  Dear Editor

  We thank Dr Derakhshan for his comments [1] regarding our report.[2]

  Dr Derakhshan discusses the hypothesis that all movements are initiated from the major hemisphere,[3] which may be closely related to handedness. In neural right handers, the command of movement may originate in the left hemisphere. In cases of left hand movement, the command originated from the dominant hemisphere is once tran...

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  Dear Editor

  We thank Dr Derakhshan for his comments [1] regarding our report.[2]

  Dr Derakhshan discusses the hypothesis that all movements are initiated from the major hemisphere,[3] which may be closely related to handedness. In neural right handers, the command of movement may originate in the left hemisphere. In cases of left hand movement, the command originated from the dominant hemisphere is once transferred to the right one via the corpus callosum, thereby producing the movement.

  Based on this hypothesis, Dr Derakhshan suggests that the left small infarct in our case may have affected a command signal from the left to the right hemisphere, thereby deteriorating the pre-existing left hemiparesis that had resulted from an earlier right putaminal haemorrhage. This discussion is interesting; however, we do not think such hypothesis can fully explain the symptoms of our case. The first- ever stroke in the dominant hemisphere rarely causes ipsilateral hemiparesis or tetraparesis. Moreover, lesion of the corpus callosum does not usually produce hemiparesis, which may be caused by the inhibition of the command transfer from the major hemisphere to the other one. In contrast, the deterioration of ipsilateral hemiparesis appears to be seen in cases of the second stroke, which occurs contralaterally to the first stroke. Thus, we feel that the reorganisation of motor control in the contralateral hemisphere after the first stroke may play an important role in the deterioration of ipsilateral hemiparesis in such cases.

  On the other hand, side of stroke may considerably influence motor recovery. In general, greater ipsilateral cortex recruitment is normally seen with left compared with right hand movement in the right handers. Such ipsilateral recruitment may increase further after brain damage.[4] Thus, there may be increasing chances that left hemiparesis improves better than right one because of the presence of the ipsilateral motor control, and that, at the same time, pre-existing left hemiparesis deteriorates when the second stroke takes place in the left hemisphere like our case. Handedness and side of stroke should be taken into consideration in discussing the process of motor recovery after stroke.

  References

  1. Derakhshan I. Making matters worse, ipsilaterally: A new explanation [electronic response to Ago et al. Deterioration of pre-existing hemiparesis brought about by subsequent ipsilateral lacunar infarction] jnnp.com 2004http://jnnp.bmjjournals.com/cgi/eletters/74/8/1152#133

  2. Ago T, Kitazono T, Ooboshi H, et al. Deterioration of pre-existing hemiparesis brought about by subsequent ipsilateral lacunar infarction. J Neurol Neurosurg Psychiatry. 2003;74:1152-1153.

  3. Kim SG, Ashe J, Hendrich K, et al. Functional magnetic resonance imaging of motor cortex: hemispheric asymmetry and handedness. Science. 1993;261:615-617.

  4. Zemke AC, Heagerty PJ, Lee C, et al. Motor cortex organization after stroke is related to side of stroke and level of recovery. Stroke. 2003;34:e23-28.

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  Conflict of Interest:
  None declared.

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• Published on: 13 April 2016

  Making matters worse, ipsilaterally: A new explanation

  • Iraj Derakhshan, Neurologist

  Dear Editor

  The Short Report by Ago and colleagues,[1] describing deterioration of pre-existing left hemiparesis by a subsequent ipsilateral hemispheric insult, contains a laterality-indexed aspect related to motor control in humans, not addressed by the authors.

  Cases similar to their patient are on record.[2] The explanation of the laterality indexed bilateral activation of motor cortices (or, as in...

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  Dear Editor

  The Short Report by Ago and colleagues,[1] describing deterioration of pre-existing left hemiparesis by a subsequent ipsilateral hemispheric insult, contains a laterality-indexed aspect related to motor control in humans, not addressed by the authors.

  Cases similar to their patient are on record.[2] The explanation of the laterality indexed bilateral activation of motor cortices (or, as in the case reported by Ago et al, activation of the cortex ipsilateral to the nondominant hand, Figure 1) is based on the fact that all movements are initiated from the major hemisphere, with those involving effectors ipsilateral to the major hemisphere requiring transfer of the command signal to the minor hemisphere via the callosum (for implementation of the signal by the minor hemisphere). This is the newly discovered anatomy of handedness.[3,4] This also is the explanation the findings in all of the articles to which the authors referred, erroneously ascribed to plasticity/reorganisation of the unaffected hemisphere. Among those articles the time-pegged EEG/EMG study by Green et al. [5] is the most instructive, documenting an average 100 ms delay when the right handed participants moved their left fingers as compared to moving the right. This delay is the interhemispheric transfer time alluded to above. Incidentally, cases 2 and 4 in Green et al.’s study were ostensible right and neural left handers wherein the timing of events were the reverse.[3- 5] (I am assuming here that Ago’s case was a right hander).

  Similarly, the nondominant delay just mentioned is inconsistent with Ago et al's suggested ipsilateral/direct corticospinal pathway; i.e. from the major hemisphere to the left side (the existence of which in humans lacks any proof).

  Thus, the worsening of the condition of the left side of their patient after a new insult to the major hemisphere was the result of diaschitic de-afferentation of the minor hemisphere from the excitatory influences originating in the major hemisphere, described elsewhere.[3,4]

  References

  1. Ago T, Kitazono H, Ooboshi H, et al. Deterioration of pre-existing hemiparesis brought about by subsequent ipsilateral lacunar infarction. J Neurol Neurosurg Psychiatry 2003; 74: 1152-1153.

  2. Nathan PW, Smith MC. Effects of two unilateral cordotomies on the motility of the lower limbs. Brain 1973; 96:471-494. (Case 103; see table 1 and pages 471, 487-488)

  3. Derakhshan I. Callosum and movement control; case reports. Neurol Res 2003; 25: 538-542.

  4. Derakhshan I, Hund-Georgiadis, von Cramon, DY. Impaired hemodynamics and neural activation? A fMRI study of major cerebral artery stenosis. Neurology 2003; Dec. 4, 2003, in press & at www.neurology.org/cgi/eletters/61/9/1276

  5. Green JB, Bialy Y, Sora E, Ricamato A, et al. High-resolution EEG in poststroke hemiparesis can identify ipsilateral generators during motor tasks. Stroke 1999; 30: 2659-2665.

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  Conflict of Interest:
  None declared.

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