Spasticity is the velocity-dependent increase in muscle tone due to the exaggeration of stretch reflex. It is only one of the several components of the upper motor neuron syndrome (UMNS). The central lesion causing the UMNS disrupts the balance of supraspinal inhibitory and excitatory inputs directed to the spinal cord, leading to a state of disinhibition of the stretch reflex. However, the delay between the acute neurological insult (trauma or stroke) and the appearance of spasticity argues against it simply being a release phenomenon and suggests some sort of plastic changes, occurring in the spinal cord and also in the brain. An important plastic change in the spinal cord could be the progressive reduction of postactivation depression due to limb immobilization. As well as hyperexcitable stretch reflexes, secondary soft tissue changes in the paretic limbs enhance muscle resistance to passive displacements. Therefore, in patients with UMNS, hypertonia can be divided into two components: hypertonia mediated by the stretch reflex, which corresponds to spasticity, and hypertonia due to soft tissue changes, which is often referred as nonreflex hypertonia or intrinsic hypertonia. Compelling evidences state that limb mobilisation in patients with UMNS is essential to prevent and treat both spasticity and intrinsic hypertonia.

It has been postulated that sensorimotor integration is abnormal in dystonia. We investigated changes in motor cortical excitability induced by peripheral stimulation in patients with focal hand dystonia (12 patients with hand cramps) and with cervical dystonia (nine with spasmodic torticollis) compared with 16 age-matched normal controls. Motor evoked potentials (MEP) to focal (figure-of-eight coil) transcranial magnetic stimulation of the hand area were recorded from the right abductor pollicis brevis (APB), first dorsal interosseus (FDI), flexor carpi radialis and extensor carpi radialis muscles. Changes of test MEP size following conditioning stimulation of the right median nerve (or of the index finger) at conditioning-test (C-T) intervals of 50, 200, 600 and 1000 ms were analysed. Peripheral stimulation significantly reduced test MEP size in the APB and FDI muscles of normal control and spasmodic torticollis patients. The inhibitory effect was larger upon median nerve stimulation and reached a maximum at the C-T interval of 200 ms. On the contrary, hand cramp patients showed a significant facilitation of test MEP size. This study suggests that MEP suppression following peripheral stimulation is defective in patients with focal hand dystonia. Central processing of sensory input is abnormal in dystonia and may contribute to increased motor cortical excitability.

Stability and mobility in functional motor activities depend on a precise regulation of phasic and tonic muscular activity that is carried out automatically, without conscious awareness. The sensorimotor control of posture involves a complex integration of multisensory inputs that results in a final motor adjustment process. All or some of the components of this system may be dysfunctional in Parkinsonian patients, rendering postural instability one of the most disabling features of Parkinson’s disease (PD). Balance control is critical for moving safely in and adapting to the environment. PD induces a multilevel impairment of this function, therefore worsening the patients’ physical and psychosocial disability. In this review, we describe the complex ways in which PD impairs posture and balance, collecting and reviewing the available experimental evidence.

The evaluation of motor cortical output after transcranial magnetic stimulation (TMS) is a means of investigating how the motor cortex reacts to external stimuli (i.e., a method to assess the excitability of the motor cortex). The recording of the descending volleys at the surface of the spinal cord provides a direct measure of the motor cortical output. However, this approach is highly invasive and can be used only during particular conditions. On the other hand, electromyographic recordings of the motor phenomena induced by TMS provide a completely painless, noninvasive, indirect measure of the cortical output, with these phenomena obviously reflecting the excitability of the spinal motoneurons as well as that of the muscle itself. The authors review how the electromyographic activity induced by TMS can provide valuable information about motor cortical excitability for use in clinical practice and research.