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.
|
Authors | U K Misra, J Kalita |
Journal | Electroencephalography and clinical neurophysiology
(Electroencephalogr Clin Neurophysiol)
Vol. 97
Issue 2
Pg. 73-6
(Apr 1995)
ISSN: 0013-4694 [Print] Ireland |
PMID | 7537206
(Publication Type: Journal Article)
|
Topics |
- Adolescent
- Adult
- Electromyography
- Extremities
(innervation)
- Humans
- Magnetic Resonance Imaging
- Male
- Muscular Atrophy, Spinal
(pathology, physiopathology)
- Neural Conduction
(physiology)
- Reaction Time
(physiology)
- Spinal Cord
(pathology)
|