Paralysis implies motor weakness, and can be partial or complete. It can result from dysfunction at any point in the motor system, and the level at which this occurs determines the characteristics of the paralysis.
Movement is initiated by specialized motor nerve cells, the upper motor neurons (sometimes called pyramidal cells, because of their shape). These cells are situated in a special part of the cerebral hemispheres, the motor cortex, and are arranged in a ‘somatotopic’ manner — which means that motor neurons subserving a particular part of the body are clustered together, and are always found in that same place. Upper motor- neurones destined to serve movements of the leg, for example, are located nearer the midline than those destined for the arms. On each side of the brain, the axons from these motor neurons converge as they leave the cerebral cortex, and pass down the brain stem as separate tracts. Just before they reach the spinal cord, most of the fibres from one side cross to the opposite side. This means that upper motor neurons on one side of the cerebral cortex control movements principally on the other side of the body. In the spinal cord they descend as a tract in the outer side part of the cord, and fibres leave the tract progressively to reach and to act on lower motor neurons (anterior horn cells), either directly or via intermediary neurons. Those destined to activate arm muscles, for example, synapse with lower motor neurons in the cervical part of the cord. From there, axons of the lower motor neurons form the motor component of the peripheral nerves, finally reaching the muscle for which they are destined. In the muscle, each nerve fibre divides into a large number of branches. A single branch innervates an individual muscle fibre at a specialized structure, the neuromuscular junction. The signal is finally passed from the nerve to the muscle by the release of a chemical substance, acetylcholine, which diffuses across the narrow gap between nerve and muscle and reacts with specialized acetylcholine receptors on the muscle fibres. This reaction leads to a local electrical potential that triggers muscle contraction.
Upper motor neuron paralysis
is characterized by stiffness of the affected muscles (spasticity) ; weakness of the muscles that extend the arm and of the muscles that flex the leg; drooping of the lower part of the face; increased tendon reflexes (the response that muscles make when their tendons are briefly tapped) ; and a positive Babinski (extensor plantar) reflex response, in which the toes move upwards when the side or sole of the foot is stroked. A common cause of an upper motor neuron paralysis is a ‘stroke’, in which either infarction (loss of blood supply) or haemorrhage in one cerebral hemisphere disrupts the motor neurons destined for the opposite half of the body. Hemiplegia is the term for such one-sided paralysis. Other causes include head injury, cerebral tumours, cerebral abscess, and also cerebral palsy in which damage occurs around the time of birth. The extent of the weakness can range from a slight interference with walking, to a paralysis so profound that the patient is chair-bound.
Upper motor neuron fibres can be damaged in their course between the brain and their lower ends by spinal cord injury: a broken neck may cause paralysis of all four limbs as well as the muscles of the torso; or a broken back, paralysis of the legs. Paraplegia is the term for such paralysis on both sides.
Lower motor neuron paralysis
has a different set of characteristics, comprising muscle wasting and weakness, loss of muscle tone, and depressed tendon reflexes. The cause can be damage to the anterior horn cells themselves (as in poliomyelitis) ; spinal injury in the lower back, where the motor nerve roots run down inside the vertebral column after leaving the spinal cord; or damage to the motor fibres in the nerves running from the spine to the muscles. Weakness can be due also to a disorder at the neuromuscular junction. In this instance it has a characteristic ‘fatiguable’ quality, in which the more the muscle is used the weaker it becomes. The muscles are not wasted. The commonest disease causing a neuromuscular transmission disorder is myasthenia gravis, in which the immune system makes antibodies to the acetylcholine receptors on the muscle fibres. The toxins of certain snakes (e.g. the banded krait) and of bacteria (e.g. botulinum toxin) also block neuromuscular transmission and paralyse their victim. Curare and the contemporary drugs developed from it cause paralysis by acting at this site: originally an arrow poison, but now a feature used to good effect (and of course reversibly) in anaesthetic practice Paralysis can also be due to muscle disease (myopathy). The weakness here usually principally affects the shoulder girdle muscles (making it difficult for the patient to elevate their arms) and the muscles of the pelvis (thereby interfering with walking). Rising from a chair or climbing stairs can be particularly difficult. Muscular dystrophies are genetic disorders, usually progressive, which can lead to profound paralysis. Other causes include inflammatory disorders (e.g. polymyositis), metabolic conditions, and toxic substances.
— J. Newsom-Davis
See also motor neuron; muscle wasting; stroke.
