[Botulinum therapy of spastic forms of cerebral palsy in various locomotor patterns]. / Botulinoterapiya spasticheskikh form detskogo tserebral'nogo paralicha pri razlichnykh lokomotornykh patternakh.

Spasticity in patients with cerebral palsy (CP) is the main impediment to normal locomotion. The function of the Central Pattern Generator (CPG), i.e. a group of neural chains in the spinal cord, stands at the core of any rhythmical movement. CPG can generate locomotion patterns without supraspinal control, which can have both positive and negative impact on the ability to move. Performing the motor tasks such as walking, running and swimming, creates the consistent rhythmical movement of legs and arms through interaction between CPGs of upper and lower extremities. This interaction can cause the activation of pathological movement patterns in lower extremities in response to upper limb spasticity. Thus, neural chains in the spinal cord become the generator of pathologically increased excitation which has developed as a result of a focal lesion in the CNS. All the statements described above show the importance of introducing the upper limb injections of bFotulinum toxin A in the protocol in order to develop normal locomotion. The PUL study approved the optimal level of efficacy and favourable safety profile of botulinum toxin A in children with CP and upper limb muscle spasticity.

Blood antidiuretic activity and selected haemodynamic indicators in patients with essential hypertension.

In patients with essential hypertension the blood antidiuretic activity was studied in relation to the haemodynamics. It was found that the blood antidiuretic activity increased in parallel with the rise in the total peripheral resistance, and with the decreases in the blood and plasma volumes, stroke volume, and end-diastolic heart volume. The role of antidiuretic hormone in the regulation of haemodynamics in hypertensive patients is discussed.

"Exaggerated" natriuresis in experimental hypertension and the role of the natriuretic factor.

In rabbits with experimental ischaemic cerebral hypertension the role of the natriuretic factor in the genesis of the phenomenon of "exaggerated" natriuresis after extracellular space expansion was studied. In control animals an expansion of the extracellular fluid was followed by an elevation of the natriuretic factor in blood, whereas in hypertensive rabbits the phenomenon did not appear. Besides, in hypertensive rabbits the urinary excretion and the clearance of the natriuretic factor were considerably higher than in the control animals. In the genesis of exaggerated natriuresis in hypertension a certain role is doubtlessly played by the natriuretic factor.

The evidence of production or activation of a natriuretic factor in the liver.

The natriuretic activity was measured with the aid of bioassay in blood flowing out from the brain, kidney and liver before and after the expansion of extracellular space in dogs. In another experiments in rats the volume natriuresis and the natriuretic activity in blood were measured in controls and in animals with carbon tetrachloride liver dystrophy and pharmacological stimulation (dehydrocholic acid, Ca pantothenate, cyanocobalamin) of liver functions. In dogs, the level of natriuretic activity in blood flowing out of the liver before and after the expansion of extracellular fluid volume was significantly higher than that in arterial blood. In contrast, the natriuretic activity was not found in the blood flowing out of the brain and the kidney. In rats the experimental dystrophy of the liver decreased the content of a natriuretic factor in blood plasma and the expansion of extracellular space did not produce any natriuretic effect as compared to control rats. After pharmacological stimulation of the liver by dehydrocholic acid, Ca pantothenate and cyanocobalamine the volume expansion led to a significant increase of the excretion of sodium by the kidney and to the increase of the content of a natriuretic factor in blood plasma as compared to control rats. These facts are considered to support the view that a natriuretic factor is either synthesized or activated by the liver.