THE MOTOR CORTEX

Voluntary motor commands begin in the motor cortex located on the outer, wrinkled surface of the brain. Movement of the right arm is begun by the left motor cortex, which generates a large volley of signals to the involved muscles. These electrical signals pass along upper motor neurons through the midbrain to the spinal cord. Within the spinal cord, they connect to lower motor neurons, which convey the signals out of the spinal cord to the surface of the muscles involved. Electrical stimulation of the muscles causes contraction, and the force of contraction pulling on the skeleton causes movement of the arm, hand, and fingers.

Damage to or death of any of the neurons along this path causes weakness or paralysis of the affected muscles.

ANTAGONISTIC MUSCLE PAIRS

This picture of movement is too simple, however. One important refinement to it comes from considering the role of opposing, or antagonistic, muscle pairs. Contraction of the biceps muscle, located on the top of the upper arm, pulls on the forearm to flex the elbow and bend the arm. Contraction of the triceps, located on the opposite side, extends the elbow and straightens the arm. Within the spine, these muscles are normally wired so that willed (voluntary) contraction of one is automatically accompanied by blocking of the other. In other words, the command to contract the biceps provokes another command within the spine to prevent contraction of the triceps. In this way, these antagonist muscles are kept from resisting one another. Spinal cord or brain injury can damage this control system and cause involuntary simultaneous contraction and spasticity, an increase in resistance to movement during motion.

THE CEREBELLUM

Once the movement of the arm is initiated, sensory information is needed to guide the finger to its precise destination. In addition to sight, the most important source of information comes from the "position sense" provided by the many sensory neurons located within the limbs (proprioception). Proprioception is what allows you to touch your nose with your finger even with your eyes closed. The balance organs in the ears provide important information about posture. Both postural and proprioceptive information are processed by a structure at the rear of the brain called the cerebellum. The cerebellum sends out electrical signals to modify movements as they progress, "sculpting" the barrage of voluntary commands into a tightly controlled, constantly evolving pattern. Cerebellar disorders cause inability to control the force, fine positioning, and speed of movements (ataxia). Disorders of the cerebellum may also impair the ability to judge distance so that a person under- or over-reaches the target (dysmetria). Tremor during voluntary movements can also result from cerebellar damage.

THE BASAL GANGLIA

Both the cerebellum and the motor cortex send information to a set of structures deep within the brain that help control involuntary components of movement (basal ganglia). The basal ganglia send output messages to the motor cortex, helping to initiate movements, regulate repetitive or patterned movements, and control muscle tone.

Circuits within the basal ganglia are complex. Within this structure, some groups of cells begin the action of other basal ganglia components and some groups of cells block the action. These complicated feedback circuits are not entirely understood. Disruptions of these circuits are known to cause several distinct movement disorders. A portion of the basal ganglia called the substantia nigra sends electrical signals that block output from another structure called the subthalamic nucleus. The subthalamic nucleus sends signals to the globus pallidus, which in turn blocks the thalamic nuclei. Finally, the thalamic nuclei send signals to the motor cortex. The substantia nigra, then, begins movement and the globus pallidus blocks it.

This complicated circuit can be disrupted at several points. For instance, loss of substantia nigra cells, as in Parkinson's disease, increases blocking of the thalamic nuclei, preventing them from sending signals to the motor cortex. The result is a loss of movement (motor activity), a characteristic of Parkinson's.

In contrast, cell loss in early Huntington's disease decreases blocking of signals from the thalamic nuclei, causing more cortex stimulation and stronger but uncontrolled movements.

Disruptions in other portions of the basal ganglia are thought to cause tics, tremors, dystonia, and a variety of other movement disorders, although the exact mechanisms are not well understood.

Some movement disorders, including Huntington's disease and inherited ataxias, are caused by inherited genetic defects. Some disease that cause sustained muscle contraction limited to a particular muscle group (focal dystonia) are inherited, but others are caused by trauma. The cause of most cases of Parkinson's disease is unknown, although genes have been found for some familial forms.