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Upper motor neuron

Upper motor neurons (UMNs) are first-order neurons located within the central nervous system that originate in the cerebral cortex and carry electrical impulses to initiate, modulate, and coordinate voluntary movements by synapsing onto lower motor neurons in the brainstem or spinal cord.^[1] These neurons form the upper segment of the motor pathway, distinguishing them from lower motor neurons, which directly innervate skeletal muscles and originate in the anterior horn of the spinal cord or cranial nerve nuclei.^[2] UMNs play a crucial role in integrating sensory and cortical inputs to enable precise motor control, with their dysfunction leading to characteristic syndromes involving weakness and spasticity rather than flaccid paralysis.^[3]

Anatomy and Pathways

The cell bodies of UMNs are primarily situated in layer V of the primary motor cortex (Brodmann area 4), particularly the large Betz cells, as well as in the premotor cortex (Brodmann area 6) and supplementary motor areas.^[2] From there, their axons descend through several key structures: the corona radiata, internal capsule, cerebral peduncles, basis pontis, and medullary pyramids, before most (approximately 90%) decussate at the pyramidal decussation in the lower medulla to form the lateral corticospinal tract.^[3] The remaining 10% cross at spinal levels to form the anterior corticospinal tract, while corticobulbar fibers target cranial nerve nuclei bilaterally for most functions, except for unilateral control of the lower face (cranial nerve VII) and tongue (cranial nerve XII).^[1] This somatotopic organization ensures that different body regions are represented in a orderly fashion along the motor cortex and tracts, facilitating targeted control of distal musculature, especially in the hands and fingers.^[3]

Function

UMNs transmit excitatory signals using glutamate as their primary neurotransmitter, synapsing directly or indirectly (via interneurons) onto lower motor neurons to activate alpha motor neurons and generate muscle contractions for voluntary actions.^[2] They integrate inputs from higher cortical areas, the basal ganglia, and cerebellum to fine-tune movement precision, inhibit unwanted reflexes, and enable skilled tasks like writing or speaking.^[1] In addition to the pyramidal (corticospinal and corticobulbar) tracts, extrapyramidal pathways involving UMNs from the brainstem contribute to posture, balance, and automatic movements, providing a complementary system for overall motor coordination.^[3] Disruption in UMN signaling, such as through inhibitory imbalances, results in the release of primitive reflexes and loss of fractionated movements.^[2]

Clinical Significance

Lesions affecting UMNs, often due to stroke, multiple sclerosis, amyotrophic lateral sclerosis (ALS), or trauma, produce upper motor neuron syndrome characterized by negative signs like paresis (weakness), loss of dexterity, and fatigue, alongside positive signs such as hyperreflexia, spasticity, clonus, and a positive Babinski reflex.^[1] The location of the lesion determines the symptoms: cortical lesions may impair motor planning and cause contralateral hemiparesis, while spinal cord involvement leads to bilateral lower limb effects below the level of injury.^[3] Corticobulbar tract damage can manifest as pseudobulbar palsy with dysarthria, dysphagia, and emotional lability.^[1] Diagnosis relies on clinical examination to differentiate UMN from lower motor neuron disorders, guiding treatments like physical therapy or medications to manage spasticity.^[2]

Anatomy

Location and Morphology

Upper motor neurons are multipolar projection neurons whose cell bodies reside primarily in layer V of the cerebral cortex, including the primary motor cortex (Brodmann area 4), premotor cortex, and supplementary motor area.^[4]^[5] These cortical upper motor neurons are distinguished from brainstem upper motor neurons, such as those in the pontine reticular formation, which contribute to extrapyramidal pathways.^[5] These neurons exhibit a classic pyramidal morphology, characterized by large, triangular somata and extensive dendritic arborization that facilitates integration of diverse cortical inputs.^[6] Betz cells, the largest subtype of upper motor neurons located in layer Vb of the primary motor cortex within the precentral gyrus, have cell body diameters ranging from 20 to 120 μm, with an average of 60–70 μm, and feature prominent apical dendrites extending superficially toward layer I alongside dense basilar dendritic arrays oriented parallel to the cortical surface.^[6] Their long axons, often myelinated and extending over a meter in humans, descend to form components of pathways like the corticospinal tract, synapsing onto lower motor neurons or interneurons in the spinal cord or brainstem.^[4] Approximately 30% of corticospinal tract fibers originate from the primary motor cortex, underscoring the prominence of this region in limb control.^[4] Cortical upper motor neurons show bilateral representation across hemispheres, but exert predominant contralateral influence on distal limb muscles via the lateral corticospinal tract, while axial and proximal muscles receive more balanced ipsilateral and contralateral input through the anterior corticospinal tract.^[7]^[8]

Synaptic Connections

Upper motor neurons establish both direct and indirect synaptic connections with lower motor neurons to facilitate motor signaling. The axons of corticospinal upper motor neurons form monosynaptic connections directly onto alpha motor neurons located in the anterior horn of the spinal cord, enabling precise control of distal musculature, particularly in the limbs.^[1] These direct synapses are characteristic of the lateral corticospinal tract and represent the primary pathway for voluntary movement initiation.^[9] While direct corticomotoneuronal connections exist, particularly for fine finger movements in primates including humans, the majority of corticospinal fibers exert influence indirectly through spinal interneurons that integrate multiple inputs for coordinated output.^[10]^[11] In addition, upper motor neurons originating from the cortex project via the corticobulbar tract to synapse directly on lower motor neurons within brainstem cranial nerve nuclei, including those for cranial nerves V (trigeminal), VII (facial), IX (glossopharyngeal), X (vagus), XI (accessory), and XII (hypoglossal).^[2] The terminals of corticospinal upper motor neuron axons primarily utilize excitatory amino acids, notably glutamate, as their neurotransmitter to depolarize postsynaptic elements in the spinal cord.^[12] Collateral branches from these axons extend to various subcortical structures for modulatory purposes, including the reticular formation in the brainstem, which receives projections to influence postural and locomotor adjustments.^[5] Additional collaterals target the red nucleus in the midbrain, contributing to rubrospinal pathways that support limb flexion, and the basal ganglia, where they interact with striatal circuits to refine motor planning and execution.^[13] These collateral projections allow upper motor neurons to integrate feedback and modulate descending signals beyond direct motor control. Upper motor neurons, primarily originating from layer V pyramidal cells in the primary motor cortex, receive convergent inputs that shape their activity.^[14] These include cortico-cortical fibers from sensory and association areas of the cortex, providing somatosensory information for movement adaptation. Thalamocortical projections from the ventrolateral thalamus relay regulatory signals from the basal ganglia and cerebellum, enabling fine-tuning of motor commands based on internal models of action.^[14] Cerebellar inputs, transmitted via the dentatothalamic tract to the thalamus and subsequently to the motor cortex, contribute to error correction and coordination in ongoing movements.^[14]

Physiology

Role in Motor Control

Upper motor neurons (UMNs) serve as the primary conduit for signals originating in higher brain centers, such as the motor cortex, to lower motor neurons (LMNs) in the spinal cord and brainstem, enabling the initiation and execution of planned voluntary movements. These neurons integrate excitatory and inhibitory inputs from cortical and subcortical regions to generate coordinated motor outputs, while also incorporating sensory feedback to refine and adjust ongoing actions in real time. This integration allows for adaptive control, where UMNs modulate LMN activity based on environmental cues and internal states, ensuring smooth and purposeful motion.^[2] A key function of UMNs is to facilitate fractionated movements, permitting independent control of individual muscles or muscle groups, particularly in distal limbs like the fingers, through direct monosynaptic connections in primates and humans. This precision supports complex tasks such as grasping or manipulating objects. Additionally, UMNs contribute to the acquisition and refinement of learned motor skills via cortical plasticity, where repeated practice reorganizes motor maps—such as the somatotopic representations in the primary motor cortex (often depicted as a homunculus)—to enhance efficiency and accuracy over time.^[15]^[5] UMNs exhibit phasic firing patterns, often increasing their discharge rate in bursts at the onset of voluntary movements to rapidly recruit LMNs and generate force. They also promote reciprocal inhibition of antagonist muscles through descending pathways that activate spinal interneurons, allowing agonist muscles to contract without opposition for efficient joint motion. Furthermore, UMNs maintain posture via tonic activity, providing steady excitatory drive to axial and proximal muscles to counteract gravity and stabilize the body during static and dynamic conditions.^[16]^[17]^[5]

Excitatory and Inhibitory Mechanisms

Upper motor neurons primarily exert excitatory influence on lower motor neurons through the release of glutamate as the neurotransmitter at their synapses. This glutamatergic transmission binds to ionotropic receptors on lower motor neurons, including α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors, leading to depolarization and facilitation of motor output. AMPA receptors mediate fast excitatory postsynaptic potentials, while NMDA receptors contribute to slower, voltage-dependent calcium influx that supports synaptic strengthening.^[2]^[18] Inhibitory mechanisms of upper motor neurons are predominantly indirect, mediated through GABAergic interneurons in the spinal cord, such as Renshaw cells, which provide recurrent inhibition to limit excessive motor neuron firing. Renshaw cells are activated by collateral axons from lower motor neurons excited by upper motor neuron input, releasing gamma-aminobutyric acid (GABA) to hyperpolarize and suppress alpha motor neurons, thereby refining motor commands. Additionally, descending inhibitory pathways from brainstem nuclei, including the reticulospinal and vestibulospinal tracts, modulate spinal excitability by targeting interneurons that inhibit lower motor neurons, contributing to overall tone regulation.^[19]^[20] Long-term potentiation (LTP) in corticospinal inputs to spinal motor circuits, including synapses with interneurons, plays a key role in motor learning by enhancing synaptic efficacy following repeated activity patterns. This Hebbian plasticity, often induced via NMDA receptor activation, strengthens connections in the corticospinal pathway to support skill acquisition and adaptation.^[21]^[22] The precise balance between excitatory and inhibitory signaling from upper motor neurons is essential to prevent pathological spasticity; disruptions, as seen in upper motor neuron lesions, lead to unopposed excitation and heightened reflex excitability.^[22] Corticospinal upper motor neurons provide the strongest excitatory drive to distal limb muscles, enabling fine voluntary control of digits and hands, whereas brainstem-derived upper motor neurons exert greater inhibitory tone on proximal muscles to maintain posture and gross movements. This differential modulation ensures coordinated action across muscle groups without interference.^[23]^[9]

Descending Pathways

Corticospinal Tract

The corticospinal tract, also known as the pyramidal tract, originates primarily from upper motor neurons in layer V pyramidal cells of the contralateral primary motor cortex (Brodmann area 4), with additional contributions from the premotor cortex, somatosensory cortex, and parietal lobe, comprising about 30% of fibers from the primary motor cortex and the remainder from supplementary and other areas.^[24]^[25] These fibers, totaling approximately 1 million myelinated axons produced by oligodendrocytes, descend through the corona radiata, posterior limb of the internal capsule, middle third of the cerebral peduncles in the midbrain, basis pontis in the pons, and medullary pyramids in the lower medulla.^[26]^[24] At the caudal medulla, the majority undergo decussation at the pyramidal decussation, where about 90% of fibers cross to the contralateral side to form the lateral corticospinal tract in the lateral funiculus of the spinal cord, while the remaining 10% stay ipsilateral to form the anterior corticospinal tract in the anterior funiculus; both tracts extend to termination levels primarily in the cervical and lumbosacral enlargements, with the lateral tract reaching lumbar segments.^[24]^[27] The tract exhibits a somatotopic organization that largely preserves the cortical homunculus arrangement, with fibers controlling the leg, arm/hand, and face positioned from medial to lateral in the motor cortex. The somatotopic organization is reorganized in the descending pathways: in the posterior limb of the internal capsule, face and hand fibers are anterior to leg fibers; in the cerebral peduncles, hand fibers are medial to leg fibers.^[28] In the spinal cord, the lateral corticospinal tract shows medial fibers innervating axial and trunk muscles for posture and proximal movements, while more lateral fibers target distal limb muscles, particularly in the upper extremity for fractionated finger movements; the anterior (ventromedial) tract, being uncrossed, primarily controls ipsilateral axial musculature.^[24]^[28] This pathway uniquely enables precise, voluntary, and skilled movements, such as independent finger dexterity and fine motor control of the hands, which are essential for dexterous manipulation in humans and distinguish it from other descending motor systems.^[24]^[25]

Brainstem Pathways

Brainstem pathways represent secondary descending motor routes originating from upper motor neurons in the brainstem, distinct from the primary corticospinal system, and primarily mediate reflexive, postural, and automatic aspects of motor control. These pathways arise from nuclei in the midbrain, pons, and medulla, descending through the brainstem tegmentum to influence spinal interneurons and lower motor neurons in the ventral horn of the spinal cord.^[29]^[30] The rubrospinal tract originates in the magnocellular red nucleus of the midbrain tegmentum and decussates immediately at the ventral tegmental decussation before descending contralaterally in the lateral funiculus of the spinal cord, terminating primarily in laminae V-VII of the ventral horn to synapse with alpha and gamma motor neurons.^[29] It facilitates flexor muscle tone and contributes to fine motor adjustments, particularly in the upper limbs, though it is less prominent in humans compared to other mammals.^[30] The vestibulospinal tract comprises lateral and medial components; the lateral arises from the lateral vestibular nucleus in the pons and descends ipsilaterally through the ventral funiculus to laminae VII and VIII, while the medial originates from the medial vestibular nucleus in the medulla and projects via the medial longitudinal fasciculus mainly to cervical levels, without decussation.^[29] These tracts support antigravity posture by exciting extensor motor neurons and inhibiting flexors, essential for balance and head stabilization.^[30] The reticulospinal tract includes medial (pontine) and lateral (medullary) divisions; the medial originates from the pontine reticular formation and descends ipsilaterally in the anterior funiculus to influence extensor tone bilaterally, whereas the lateral arises from the medullary gigantocellular reticular nucleus, partially decussates, and travels in the lateral funiculus to modulate both flexors and extensors.^[29] It plays a key role in locomotion, posture, and the coordination of axial and proximal limb movements.^[30] The tectospinal tract, a minor pathway, originates in the superior colliculus of the midbrain tectum, decussates in the midbrain, and descends ventromedially through the anterior funiculus to terminate in the contralateral cervical and upper thoracic ventral horn (laminae VI-VIII).^[29] This tract coordinates reflexive head, neck, and eye movements in response to visual or auditory stimuli.^[30] Collectively, these brainstem pathways enable automatic movements, provide anti-gravity support, and modulate spinal reflexes by integrating sensory inputs and influencing local spinal circuits, often in concert with basal ganglia outputs that project to brainstem nuclei for refined automatic motor control.^[31] They interact with the corticospinal tract through collateral projections, allowing for coordinated modulation of voluntary and reflexive actions.^[29]

Clinical Significance

Lesion Characteristics

Upper motor neuron lesions encompass a range of pathological etiologies that disrupt the descending motor pathways originating from the cerebral cortex and brainstem. Vascular causes, such as ischemic or hemorrhagic strokes in territories like the middle cerebral artery, are common precipitants, leading to acute infarction of UMN cell bodies or fibers.^[1] Traumatic injuries, including head trauma or spinal cord contusions, can directly damage UMN structures through mechanical disruption.^[2] Degenerative processes, exemplified by amyotrophic lateral sclerosis (ALS) and primary lateral sclerosis, progressively involve UMN degeneration via protein aggregation and excitotoxicity.^[1] Demyelinating conditions like multiple sclerosis impair UMN function through immune-mediated myelin loss and axonal damage in the central nervous system.^[2] The clinical syndrome arising from these lesions, known as upper motor neuron syndrome, features distinct positive and negative motor signs. Positive signs include hyperreflexia, characterized by exaggerated deep tendon reflexes due to unopposed spinal reflex activity; spasticity, a velocity-dependent resistance to passive muscle stretch resulting from heightened excitability of the stretch reflex arc; clonus, rhythmic oscillations of muscle contraction at 5-7 Hz elicited by sustained stretch; and a positive Babinski sign, where stroking the plantar surface causes dorsiflexion of the big toe and fanning of the other toes.^[32] Negative signs manifest as weakness or paresis, predominantly in antigravity muscles such as arm extensors and leg flexors, with preserved muscle bulk initially and absence of fasciculations.^[1] Mechanistically, UMN lesions interrupt descending inhibitory pathways that normally modulate spinal interneurons and motor neurons, resulting in disinhibition of segmental reflexes and enhanced gamma motor neuron activity.^[32] Acutely, especially in spinal cord injuries, this often produces an initial flaccid phase with hypotonia and hyporeflexia, known as spinal shock, lasting days to weeks, before transitioning to the chronic spastic state as supraspinal influences recover and excitatory drive predominates.^[1] Lesion location dictates the laterality and distribution of deficits: those rostral to the medullary pyramidal decussation, such as in the cerebral cortex, yield contralateral hemiparesis affecting the body below the lesion level.^[2] Brainstem lesions, occurring rostral to or at the decussation, often produce ipsilateral cranial nerve involvement alongside contralateral body signs due to the uncrossed corticospinal tract and the local position of cranial nerve nuclei.^[1] These patterns arise primarily from interruption of the corticospinal tract, a key descending pathway conveying voluntary motor commands.^[32]

Associated Disorders

Upper motor neuron (UMN) disorders encompass a range of conditions characterized by progressive or acute degeneration or damage to these neurons, leading to motor impairments such as spasticity and weakness. Primary lateral sclerosis (PLS) represents a pure form of UMN degeneration, a rare neurodegenerative disorder with an insidious onset of symptoms including spasticity, hyperreflexia, and mild weakness, while sparing lower motor neurons (LMNs).^[33] PLS typically progresses slowly over years, with symptoms often beginning in the legs and spreading to the arms and bulbar regions, and it accounts for approximately 1-3% of all motor neuron diseases.^[34] Amyotrophic lateral sclerosis (ALS) frequently involves mixed UMN and LMN pathology, though UMN-predominant variants exhibit a slower disease progression compared to classic ALS, with patients often surviving longer due to delayed involvement of respiratory muscles.^[35] The incidence of ALS is approximately 2 per 100,000 individuals annually, with UMN signs such as hyperreflexia and spasticity serving as hallmarks in predominant cases.^[36] Cerebral palsy, particularly the spastic subtype, arises from perinatal UMN lesions, often due to hypoxic-ischemic events or vascular insults, resulting in lifelong nonprogressive motor dysfunction affecting about 1 in 500 neonates.^[37] Stroke-induced hemiplegia, another common UMN disorder, stems from acute cerebrovascular events damaging the corticospinal tract, leading to contralateral weakness and spasticity that may partially recover with rehabilitation.^[32] Diagnosis of UMN disorders relies on clinical examination, including elicitation of the Hoffmann sign—an involuntary thumb flexion upon flicking the middle finger's nail—which indicates corticospinal tract dysfunction.^[38] Magnetic resonance imaging (MRI) is essential for localizing lesions, such as cortical atrophy in PLS or infarcts in stroke, while electromyography (EMG) helps differentiate UMN from LMN involvement by confirming the absence of denervation patterns.^[1] Therapeutic approaches for UMN disorders are primarily symptomatic, focusing on managing spasticity and maintaining function. Baclofen, a GABA-B agonist, effectively reduces spasticity through intrathecal or oral administration, improving mobility in conditions like PLS and post-stroke hemiplegia. Physical therapy plays a crucial role in preventing contractures and enhancing motor control across these disorders. For ALS, riluzole provides neuroprotection by modulating glutamate release, modestly extending survival by 2-3 months in UMN-predominant cases. Emerging treatments include stem cell therapies, with phase II trials as of 2025 demonstrating potential for cortical UMN repair through mesenchymal stem cell transplantation, though long-term efficacy remains under evaluation. Gene therapies targeting SOD1 mutations, responsible for about 2% of sporadic and 20% of familial ALS cases, have advanced with tofersen (an antisense oligonucleotide) approval in 2023, showing sustained stabilization of disease progression and reduced neurofilament light chain levels in treated patients.^[39]

Comparison to Lower Motor Neurons

Structural Differences

Upper motor neurons (UMNs) are located entirely within the central nervous system (CNS), with their cell bodies residing in layer 5 of the primary motor cortex (precentral gyrus), as well as in premotor and supplementary motor areas, from where their axons descend via pathways such as the corticospinal tract to synapse with interneurons or lower motor neurons (LMNs) in the spinal cord or brainstem.^[2] In contrast, LMNs have their cell bodies situated in the anterior (ventral) horn of the spinal cord or in the motor nuclei of cranial nerves within the brainstem, extending axons into the peripheral nervous system (PNS) to directly innervate skeletal muscles.^[40] This fundamental locational distinction—UMNs confined to the CNS versus LMNs bridging the CNS-PNS interface—underpins their divergent structural organizations and connectivity patterns.^[2] The axons of UMNs are notably long, often extending up to approximately 1 meter from the cerebral cortex to the lumbar or sacral regions of the spinal cord, and are myelinated by oligodendrocytes within the CNS, which form multiple internodes along a single axon to facilitate saltatory conduction.^[41] These axons do not form neuromuscular junctions, instead terminating in synaptic connections onto LMNs or interneurons, thereby exerting indirect control over muscle activity without direct peripheral innervation.^[2] LMN axons, by comparison, are shorter, typically spanning from the spinal cord or brainstem to nearby skeletal muscles (e.g., tens of centimeters in the limbs), and their peripheral segments are myelinated by Schwann cells, which ensheath a single axon segment per cell and produce nodes of Ranvier flanked by microvilli for enhanced signal propagation in the PNS.^[42] Unlike UMNs, LMNs establish direct neuromuscular junctions at the muscle endplate, enabling precise, one-to-one transmission to effector tissues.^[40] A key structural feature of LMNs is their role in forming motor units, where a single alpha motor neuron innervates a specific group of a few (e.g., 10-20) to over 2000 muscle fibers, depending on the muscle; smaller numbers in fine-control muscles like those of the eye, larger in postural muscles like the gastrocnemius.^[41] UMNs, lacking direct muscle innervation, influence broader populations of LMNs and interneurons, resulting in a more distributed structural impact rather than discrete motor units.^[2] Consequently, pure UMN lesions do not lead to denervation atrophy of muscles, as LMNs remain intact and continue providing trophic support to muscle fibers, distinguishing this from the rapid atrophy seen in LMN damage.^[32] Morphologically, many cortical UMNs, such as Betz cells, exhibit a large pyramidal shape with extensive apical dendrites branching into layer 1 of the cortex, adapted for integrative processing within the CNS.^[2]

Functional Distinctions

Upper motor neurons (UMNs) primarily function in the higher-order planning and integration of voluntary motor intent, coordinating movements through descending pathways from the cerebral cortex and brainstem to modulate spinal cord circuits. In contrast, lower motor neurons (LMNs) serve as the direct effectors for muscle contraction, transmitting signals from the spinal cord or brainstem nuclei to skeletal muscles via peripheral nerves. This division allows UMNs to integrate sensory feedback, cognitive inputs, and reflexive adjustments for smooth, purposeful actions, while LMNs execute the final output without further processing. A key functional distinction lies in the role of UMNs in supraspinal modulation of spinal reflexes, where they exert both excitatory and inhibitory influences on LMNs to refine motor responses and prevent excessive muscle activity. LMNs, however, represent the "final common path" for all motor outputs, as they converge inputs from multiple sources—including UMNs, interneurons, and sensory afferents—to innervate individual muscle fibers, ensuring precise force generation. This concept, introduced by Charles Sherrington, underscores how LMNs act as the obligatory conduit for any voluntary or reflexive movement, without the integrative capacity of UMNs. Lesions in UMNs disrupt this higher-level control, leading to spastic paresis characterized by increased muscle tone, hyperreflexia, and a velocity-dependent resistance to passive movement due to loss of inhibitory modulation on spinal reflexes. Conversely, LMN lesions result in flaccid paralysis, with hypotonia, hyporeflexia or areflexia, fasciculations, and eventual muscle atrophy from denervation, as the direct neural supply to muscles is severed. In UMNs, reflexes are often preserved or exaggerated because of disinhibition of spinal circuits, whereas LMN damage abolishes them entirely by interrupting the arc at the effector level. Clinical implications highlight these distinctions in mixed lesions, such as in amyotrophic lateral sclerosis (ALS), where both UMN and LMN involvement produces a combination of spasticity and flaccidity, hyperreflexia alongside atrophy and fasciculations, aiding in differential diagnosis. While UMNs enable adaptive motor behaviors through central nervous system processing, LMNs ensure reliable peripheral execution, and their complementary roles are evident in the contrasting patterns of dysfunction following selective injury.

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Signals from the axon and the extracellular matrix drive Schwann cells to adopt a myelinating fate. In turn, myelination reorganizes the axon for its role in ...
[41]
[PDF] clinical implementation of nerve cuff electrodes
Each motor neuron innervates 100-1000 muscle fibers (Kandel, Schwartz et al. 2000) so damage to neural tissue results in a more significant loss than damage ...