Presynaptic inhibition of Ia terminals and postactivation depression at the Ia fibre-motor neuron (MN) synapses were compared in the upper and lower limbs of both sides in subjects from different populations: 49 spastic patients with hemiplegia [mainly with a lesion in the middle cerebral artery (MCA) area], two tetraplegics and 35 healthy subjects. Presynaptic inhibition was assessed using D1 inhibition of the soleus and the flexor carpi radialis (FCR) H reflexes elicited by electrical stimuli applied to the nerve supplying antagonistic muscles, and postactivation depression was explored by varying the time interval between two consecutive H reflexes. In normal subjects no right-left asymmetry was found in the amount of presynaptic Ia inhibition, homosynaptic depression or the H(max)/M(max) ratio. In the hemiplegic side of patients with MCA area lesions, the H(max)/M(max) ratio was significantly increased in the soleus but not in the FCR. Presynaptic inhibition of Ia terminals, which was significantly reduced at the cervical level on the hemiplegic side (and also, but to a lesser extent, on the unaffected side), was unchanged at the lumbar level. Homosynaptic depression was similarly reduced at the cervical and lumbar levels on the hemiplegic side but not modified on the unaffected side. It is argued that the decrease in presynaptic inhibition of Ia terminals is more a correlate of spasticity than a mechanism underlying it. The decrease in postactivation depression, which very probably contributes to the exaggeration of the stretch reflex characterizing spasticity, might be a consequence of the changes in the pattern of activation of Ia afferents and MNs following the motor impairment.

Neurological complications of PSS are frequent since they were present in 40% (10/25) of patients in a consecutive series of patients from a department of Internal Medicine. Although PNS involvement predominates, complications of PSS affecting the brain or spinal cord are not rare, with subcortical dysfunction as the main finding.

1. Interneurones mediating reciprocal inhibition between wrist flexors and extensors in man are characterized using both Renshaw cells and transarticular group I afferent activation. 2. Renshaw cells were activated by reflex discharges evoked by a tendon tap. The tendon tap was applied to the tendon of the muscles from which the Ia fibres responsible for the reciprocal inhibition originated. Contrary to what was observed both in the cat hindlimb and in human elbow muscles, this Renshaw cell activation never resulted in a long depression of the reciprocal inhibition between wrist flexors and extensors. 3. Convergence from group I elbow muscle afferents and antagonistic group I afferents onto interneurones mediating reciprocal inhibition between wrist muscles was revealed in post‐stimulus time histogram (PSTH) experiments using the technique of spatial facilitation. 4. The characteristics of the interneurones mediating reciprocal inhibition between wrist flexors and extensors could therefore be summarized as follows: (a) they are fed by antagonistic group I afferents and group I afferents originating from both flexor and extensor elbow muscles; (b) they are not inhibited by Renshaw cells; (c) they are not excited by low threshold cutaneous afferents; and (d) they are probably interposed in a disynaptic pathway. 5. It is therefore concluded that interneurones mediating reciprocal inhibition between wrist flexors and extensors in man differ both from Ia interneurones and from interneurones interposed in the Ib reflex pathways and these characteristics are related to the complex circumduction movements developed in the wrist.

A migrainous patient who experienced chest pain attributed to engine pectoris by coronary artery spasm during a migraine attack is reported. Previous reports have already mentioned the association of these two conditions and suggested that it might be the manifestation of a generalized vasospastic disorder. This new report offers an opportunity to review and discuss the available data on such an association. Key words: migraine, coronary artery spasm Abbreviations:APCS angina pectoris due to coronary artery spasm (Headache 1996;36:332-334) Several reports have been published on the association of migraine and angina pectoris due to coronary artery spasm (APCS). [1][2][3][4] The simultaneous occurrence of these two conditions has been ascribed by some authors to a common disorder involving vascular tone. [2][3][4][5][6] We report the history of a migrainous patient who presented with a retrosternal pain during an attack of migraine with aura. According to the electrocardiogram changes and the normality of the coronary arteriography, the retrosternal pain was attributed to APCS. We propose a review of the literature and try to evaluate the arguments in favor of either a casual or specific association of APCS and migraine. CASE HISTORYA 40-year-old man had had migraine attacks since the age of 12. Each began with an aura involving blurred vision in the left visual field followed by progressive ascending paresthesias of the left hand and foot extending to the whole left upper and lower limb over the course of an hour. Afterwards, a pulsating frontal headache developed accompanied by photophobia, phonophobia, and nausea. Each attack lasted 1 day. Since the age of 18, he had had approximately one attack every 6 months. One ergotamine-caffeine tablet was able to abort an attack. The patient had no other significant past history or cardiovascular risk factors. His maternal grandmother and great uncle, as well as his own daughter, had similar migraine attacks.On November 2, 1992 at 11 AM the patient noted his usual migraine prodromes. Since he did not have any ergotamine-caffeine with him, the attack followed its usual course. When the headache was at its worst, he was at rest and suddenly experienced severe, constrictive, retrosternal chest pain with malaise.At noon, clinical examination demonstrated intense pallor, reduced level of consciousness, and a mild sensorimotor deficit of the left upper and lower limb. Deep tendon reflexes were normal, and there was no Babinski's sign. The heart rate was 77 beats per minute and the blood pressure 130/ 70 mm Hg. The rest of the examination was normal.At the same time, the electrocardiogram (ECG) showed a normal sinus rhythm with ST segment elevation in leads V1, V2, and V3 (Figure 1). The serum electrolytes, full blood count, and coagulation tests were normal. The creatine kinase (CK) level was 200 U/L (normal 30 to 130 U/L); CK isoenzymes were not done.Sublingual nitroglycerin rapidly relieved the chest pain. The ECG abnormalities suggested the diagnosis of APCS. A coronary...