Paralysis
Paralysis is the loss of muscle function in part or all of the body, occurring when nerve signals from the brain to the muscles are disrupted or interrupted.[1] As of 2013, approximately 5.4 million people in the United States (about 1 in 50) live with some form of paralysis.[2] This condition can be complete, resulting in no movement or sensation, or partial (known as paresis), where some muscle control remains.[3] It may affect a single area, one side of the body, or multiple limbs, and can onset suddenly, as in a stroke, or develop gradually due to progressive diseases.[3] Paralysis manifests in various types based on the extent and location of the impairment. Common forms include monoplegia, affecting one limb; hemiplegia, involving one side of the body; paraplegia, which paralyzes the lower body including the legs; and quadriplegia (or tetraplegia), impacting all four limbs and the trunk.[3] Muscle tone in paralyzed areas can be spastic, characterized by stiffness and involuntary spasms often seen in conditions like cerebral palsy, or flaccid, featuring limp, atrophied muscles as in poliomyelitis.[3] More localized types include Bell's palsy, causing temporary facial weakness, and vocal cord paralysis, which affects voice production.[4][5] The primary causes of paralysis stem from damage to the nervous system, including traumatic injuries to the spinal cord such as those from vehicle accidents (accounting for nearly half of new spinal cord injuries) or falls, particularly in older adults.[6] Non-traumatic origins include strokes, infections like polio (now rare in the U.S. due to vaccination), multiple sclerosis, amyotrophic lateral sclerosis (ALS), and congenital conditions such as spina bifida.[1][3] Symptoms typically involve loss of voluntary movement, numbness, tingling, muscle weakness, pain, or changes in bowel and bladder control below the affected area; in severe spinal injuries, breathing difficulties may also occur.[6][3] Treatment focuses on addressing the underlying cause and managing symptoms, as permanent paralysis often lacks a cure.[3] Options include medications like steroids for inflammatory conditions such as Bell's palsy, physical therapy for rehabilitation, functional electrical stimulation to activate muscles, and assistive devices like wheelchairs or orthotics.[3] For spinal cord injuries, emergency stabilization and surgical intervention can prevent further damage, while ongoing research explores regenerative therapies.[6] Early intervention is critical to improve outcomes and quality of life.[7]Definition and Classification
Definition and Pathophysiology
Paralysis is defined as the complete loss of voluntary muscle function, resulting in an inability to move affected body parts, whereas paresis refers to partial loss of muscle strength or weakness. This condition arises from the interruption of motor pathways that transmit signals from the central nervous system to skeletal muscles.[8][9] The pathophysiology of paralysis involves disruption of neural pathways at various levels, preventing the propagation of action potentials necessary for muscle contraction. In the central nervous system, upper motor neuron (UMN) lesions occur above the anterior horn cells of the spinal cord or cranial nerve nuclei, affecting descending tracts such as the corticospinal and corticobulbar pathways that originate in the cerebral cortex and travel through the brainstem and spinal cord. These lesions lead to spastic paralysis, characterized by increased muscle tone, hyperreflexia, and clonus due to the loss of inhibitory control over spinal reflexes. In contrast, lower motor neuron (LMN) lesions involve damage to neurons in the spinal cord's anterior horn or cranial nerve nuclei, or their peripheral axons, resulting in flaccid paralysis with muscle atrophy, fasciculations, and hyporeflexia because of direct denervation of muscles. Key anatomical structures implicated include the brain (motor cortex), spinal cord, peripheral nerves, and the neuromuscular junction, where any interruption halts signal transmission.[10][11][12] Neural signaling for voluntary muscle movement begins with action potentials generated in upper motor neurons in the cerebral cortex, which synapse with lower motor neurons in the spinal cord or brainstem via excitatory neurotransmitters. Lower motor neurons then propagate these signals through peripheral nerves to the neuromuscular junction, where acetylcholine is released into the synaptic cleft and binds to nicotinic receptors on the muscle endplate. This binding opens ligand-gated ion channels, allowing sodium ions to influx and cause membrane depolarization from approximately -90 mV to -40 mV, generating an endplate potential that triggers voltage-gated sodium channels to initiate a muscle action potential. The action potential spreads along the muscle fiber membrane and into T-tubules, prompting calcium release from the sarcoplasmic reticulum; calcium ions bind to troponin, enabling actin-myosin cross-bridge formation and muscle contraction. Disruption at any point—such as in synaptic transmission or ion channel function—prevents depolarization and subsequent contraction, leading to paralysis.[13][14][15]Types of Paralysis
Paralysis is classified primarily by the location and extent of affected body parts, providing a framework for understanding its impact on mobility and function. The main types include monoplegia, which involves paralysis of a single limb; hemiplegia, affecting one side of the body; paraplegia, limited to the lower limbs and trunk; and quadriplegia (also known as tetraplegia), encompassing all four limbs and often the trunk.[3][16] Another key classification distinguishes paralysis by its characteristics, particularly muscle tone and reflex activity, dividing it into flaccid and spastic forms. Flaccid paralysis features low muscle tone, resulting in limp, floppy muscles with absent or diminished reflexes, often presenting as weakness without resistance to passive movement.[17][18] In contrast, spastic paralysis involves increased muscle tone, leading to stiff, rigid muscles with exaggerated reflexes and involuntary contractions, such as clonus; this form arises from disruptions in upper motor neuron pathways, enhancing stretch reflexes.[17][19]| Aspect | Flaccid Paralysis | Spastic Paralysis |
|---|---|---|
| Muscle Tone | Decreased (limp, floppy) | Increased (stiff, rigid) |
| Reflexes | Absent or reduced | Exaggerated or hyperactive |
| Appearance | Soft, weak muscles without resistance | Tense muscles with possible spasms |