Central motor conduction in Hirayama disease

Electroencephalography and Clinical Neurophysiology
U K Misra, J Kalita

Abstract

The pathogenesis of Hirayama disease is usually attributed to microcirculatory disturbances in the anterior spinal artery territory, leading to segmental anterior horn cell loss and occasional lower limb hyperreflexia. In 7 patients with Hirayama disease, central motor conduction to upper (CMCT-ADM) and lower limbs (CMCT-TA) was evaluated. CMCT-TA was normal in all, but CMCT-ADM was marginally prolonged (8.4 msec, amplitude 0.8 mV) on one side only. Peripheral delay in the upper limbs was found in 2 patients (1 side each) which might be due to fall-out of anterior horn cells. In 2 patients with lower limb hyperreflexia, HM ratio, vibratory inhibition and reciprocal inhibition of soleus H reflex were also normal, suggesting lack of pyramidal dysfunction. Our results do not suggest any pyramidal dysfunction as a cause of lower limb hyperreflexia in Hirayama disease.

References

Aug 1, 1994·Electroencephalography and Clinical Neurophysiology·U K Misra, C M Pandey
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Citations

Oct 23, 2008·Neurological Sciences : Official Journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology·Angelo AmmendolaGioacchino Tedeschi
Nov 1, 1996·Clinical Neurology and Neurosurgery·U K Misra, J Kalita
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Feb 25, 1999·Electroencephalography and Clinical Neurophysiology·R MassaG Bernardi
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