Injury to the Reticular Formation Can Result in Which of the Following?

Introduction

The reticular formation is a circuitous network of brainstem nuclei and neurons that serve every bit a major integration and relay eye for many vital encephalon systems to coordinate functions necessary for survival. The structure of the reticular formation forms a internet-similar connection of nuclei and neurons, hence its name "reticular," which correlates to its office of integrating, coordinating, and influencing various regions of the key and peripheral nervous systems, both rostrally and caudally through a series of tracts. The reticular formation does not contain distinct boundaries, and the many nuclei included in this structure do not have precise delineations of territory, making the reticular formation a difficult structure to narrate and study. The widespread and lengthened nature of the reticular germination makes studies that rely on the devastation of a specific brain region difficult, and instance studies of human being brainstem injury do not but impact the reticular formation in isolation. These challenges inherent to the report of the reticular formation leave many questions to be answered and provide for future research opportunities.[1]

Structure and Role

The reticular germination is made up of a cyberspace-like construction of various brainstem nuclei and neurons and covers an expansive portion of the brainstem, kickoff in the mesencephalon, extending caudally through the medulla oblongata, and projecting into the superior cervical spinal cord segments. The reticular germination does not have any distinct cytoarchitectural boundaries and is dispersed throughout the brainstem equally a network of interconnected neurons with many projections rostrally to subcortical and cortical brain structures besides every bit caudally to the spinal string. Despite having non-distinct borders, the reticular germination contains over 100 individual brainstem nuclei.[2] Inside this vast assortment of neuronal connections, there are related just singled-out brainstem nuclei, such as the red nucleus and the nucleus reticularis tegmenti pontis, embedded in the reticular network. Due to the expansive network of tracts and the interconnected structure, the reticular formation functions equally an integration, relay, and coordination center for many vital life functions and controls many of the protective reflexes.[3]

Although at that place are no distinct borders of the reticular formation, many of its functions accept been localized and correlated with full general areas of the brainstem. Past dividing the reticular formation into dissimilar areas based on their orientation caudally, rostrally, medially or laterally, certain areas tin correlate with neuronal prison cell types and various functions discovered through various experiments on animal models equally well as human example studies.[2] Many of the neurons in the reticular formation are multi-modal and respond to various modalities of stimuli, allowing them to integrate many different types of senses and relay them to college cortical areas.[4] Interneurons that brand up the vast majority of the neuronal population in the reticular formation allow for this vast connectivity. Each neuron within the reticular formation makes synapses with many other secondary neurons, causing an exponential number of connections to form the network-like structure.[2]

The reticular formation, through its vast array of projections and networks, functions to coordinate many reflexive and vital functions. The major functions that the reticular formation influences are arousal, consciousness, circadian rhythm, slumber-wake cycles, coordination of somatic motor movements, cardiovascular and respiratory control, pain modulation, and habituation. Cardiovascular command, in specific, is modulated by the vasomotor center present in the medulla oblongata.[two] The cardinal areas, which inquiry has determined to play a role in the autonomic rhythms of respiration, are located caudally in the reticular formation well-nigh the junction of the pons and the medulla. These centers are too associated with the cranial nerve motor nuclei of the trigeminal, facial, glossopharyngeal, vagus, and hypoglossal nerves to coordinate the circuitous task of respiration.[5]

Dividing the Reticular Formation in the Medial to Lateral Orientation

The reticular formation present in the pons and medulla can split into lateral and medial tegmental fields, each associated with a dissimilar neuronal population and function. The lateral tegmental field of the reticular formation contains mostly populations of interneurons, which is the major cell type nowadays throughout the entirety of the reticular formation. These interneurons in the lateral tegmental field influence many of the cranial nerve motor nuclei (trigeminal, facial, vagal, and hypoglossal), too as form projections to diverse structures of the limbic system. Also, in the lateral tegmental field, premotor neurons are present that projection via long descending axons to spinal cord motor neurons, which participate in many of the autonomic functions necessary for survival, such every bit respiration, regulation of abdominal pressure level and function, micturition, and regulation of blood pressure. In dissimilarity, the medial tegmental field of the reticular germination has the function of coordinating eye and head movements and integrating these movements with other somatosensory, vestibular, and proprioceptive stimuli through descending axonal tracts.[three]

The reticular formation tin can also divide into 3 columns based on their neuronal construction and function. These three columns from medial to lateral are the raphe nuclei, located in the midline of the reticular formation core, the gigantocellular reticular nuclei more laterally, and the parvocellular reticular nuclei, which comprises the most lateral aspect of the column organization. The raphe nuclei form a primal ridge of the reticular formation and play an important role in mood regulation and arousal through neurotransmission via serotonin and projections to the limbic regions. The medial cavalcade of the gigantocellular reticular nuclei is composed of larger neurons and coordinates motor movements. The virtually lateral of the columns comprising the parvocellular nuclei contain smaller neurons and are known to regulate respiratory function, specifically exhalation. The lateral aspects of the reticular formation besides are close to various cranial nerves and piece of work to attune their motor function.[2]

The Ascending and Descending Tracts of the Reticular Formation

Many projections arise from the reticular germination and either ascend to subcortical and cortical regions of the brain or descend to other areas of the brainstem and spinal cord, allowing the reticular formation to play a major part as an integration and relay eye. The major ascending pathway is known as the ascending reticular activating system and plays a role in establishing alertness, arousal, consciousness, slumber-wake cycles, and circadian rhythm. The ascending reticular activating organisation has a neuronal population consisting of more often than not dopaminergic, noradrenergic, serotonergic, histaminergic, cholinergic, and glutamatergic encephalon nuclei, which accept projections to the thalamus and cerebral cortex, primarily the prefrontal cortices. A major regulatory organisation of the ascending reticular activating system is the lateral hypothalamus. This region of the brain contains orexin neurons, which are fundamental neurons in the coordination of alacrity and sleep-wake cycles. Damage to this region of the brainstem results in reductions in the level of consciousness and progression to coma in many patients. If lesions affect the ascending reticular activating system bilaterally at the level of the midbrain, death tin issue. The ascending reticular activating arrangement is also responsible for the miracle of habituation. This procedure allows the brain to ignore stimuli that are repetitive and meaningless and diverts focus to more than important and changing stimuli in the environment.[2]

The reticulospinal tracts are the major descending pathways from the reticular formation and act on many levels of the spinal string to coordinate movements and autonomic functions. The reticulospinal tracts project to spinal cord motor neurons and assistance to modulate tone, balance, posture, and coordination of body movements with the assistance of other sensory stimuli, such equally visual, auditory, vestibular, and proprioceptive information. In the lateral system of the descending reticulospinal tract are the corticospinal and rubrospinal tracts, which modulate fine movement control. The medial system of the descending reticulospinal tracts is composed of the reticulospinal pathway and the vestibulospinal pathway, major players in coordination posture. This reticulospinal pathway farther divides into the medial pontine and the lateral medullary reticulospinal tracts, each having a unique function. The medial pontine reticulospinal tract controls extensor musculature. The lateral medullary reticulospinal tract functions to inhibit excitatory centric extensor muscles as well as control autonomic functions of breathing.[2]

These descending pathways of the reticular formation play a major part in maintaining appropriate posture. If there is damage to the reticulospinal tract in the pons or medulla or the vestibulospinal tract, patients can experience postural instability and ataxia. Damage, which disrupts the normal signaling of the vestibular nuclei in the pons from the cerise nucleus located in the midbrain, may cause decerebrate posturing, causing the arms and legs to extend and internally rotate in response to painful stimuli, with hyperreflexia and hypertonic muscles. Impairment to the brainstem above the scarlet nucleus may crusade decorticate posturing, in which the arms remain flexed towards the core of the body, and the legs extend in response to painful stimuli. Damage below the vestibular nuclei in the medulla may lead to hypotonia, hyporeflexia, flaccid paralysis of the limbs and body, quadriplegia, and loss of the respiratory drive. This miracle is chosen spinal shock, and patients feel these symptoms because of the loss of tonic activity from both the lateral vestibulospinal and reticulospinal tracts, which normally influence peripheral motor neurons.[2] In that location are also some areas of the reticular germination whose axons bifurcate and send signals in both the ascending and descending tracts. These areas are by and large situated in the rostral part of the midbrain and send projections to the hypothalamus, basal ganglia, and septal areas.[ane]

Dividing the Reticular Formation in the Rostral to Caudal Orientation

Another way of dividing the reticular formation into vague functional areas is in the rostral to caudal orientation. The functions of the reticular formation that are more modulatory in nature are generally controlled past the rostral sections, while the caudal sections control the premotor functions. The rostral and caudal orientation of the reticular formation also determines the relative contribution of the medial and lateral columns. As one examines the reticular formation columns moving from a rostral department more caudally, the medial reticular formation column becomes less prominent, and the lateral column becomes more prominent. Brute studies that examined the bear upon of lesions on various areas of the reticular formation demonstrated that rostral lesions produced hypersomnia and caudal lesions produced insomnia in cat models. Many studies such equally these have taken identify showing contradictory behaviors in the diverse regulatory functions of the reticular formation based on the location of the lesions, demonstrating its prominent office in modulation, integration, and coordinating diverse systems throughout the body.[2]

Pain Modulation

Another important function of the reticular formation is in the modulation of pain stimuli. For hurting from the periphery to attain the cerebral cortex to exist brought to witting attention, pain signals travel through the reticular activating system through an ascending tract. The reticular activating arrangement also projects descending pathways that play a office in the analgesic pain pathway, modulating the awareness of pain in the periphery and blocking manual from the spinal cord to the cortex. The analgesic pain pathway works through the gate-control mechanism present in the spinal cord, in which presynaptic inhibition of pain stimulation occurs in zone Ii of the substantia gelatinosa of the spinal cord before it can be transmitted to a secondary neuron and ascend to the cerebral cortex via the spinothalamic tract.[ii] The thought is that nociceptive stimuli reaching the reticular germination are responsible for the many behavioral and defensive responses to pain. Prove also suggests that these ascending pain signals reaching the reticular germination in the medulla also play a modulatory function in autonomic function with a major bear on on cardiovascular control as well every bit motor control as role of the flight or fight sympathetic reaction.[six]

Understanding the hurting and analgesic pathways that are modulated by diverse regions of the cognitive cortex, brainstem, and spinal cord tin provide crucial insights into the phenomenon of neuropathic pain. The thought is that since the reticular formation and other hurting modulating regions of the brain have extensive connections to the limbic and memory centers, chronic central pain can persist despite the cessation of the noxious peripheral stimulus. Some other important phenomenon relates to the reticular formations' contribution to pain post-obit spinal cord injuries. Due to the diffuse location and multi-synaptic network of the reticular formation, information technology rarely is completely destroyed afterwards a spinal cord injury, allowing for pain pathways to the cerebral cortex to persist and contributing to substantial hurting and discomfort. This condition can also lead to the misinterpretation of non-painful sensations below the level of the spinal cord injury to travel through the hurting conducting ascending pathways of the reticular formation, resulting in the phenomenon of allodynia.[2][6]

Ocular Responses

The reticular formation also plays a vital role in centre gaze, coordination of centre saccades, and head motion. Different parts of the reticular formation are responsible for various ocular functions. The mesencephalic reticular germination coordinates vertical gaze, the paramedian pontine reticular formation coordinates horizontal gaze, and the medullary pontine reticular formation coordinates head movements and gaze holding. These regions directly projection to the extraocular motor nuclei and are essential for saccadic eye movements. These centers also take connections via the descending reticulospinal neurons to coordinate posture and cervix movements with the centre movements.[3][7]

Embryology

The evolution of the central nervous system, which comprises the brain, brainstem, and spinal cord, initiates at gestational week three and continues afterwards birth until late boyhood and potentially throughout the entire lifespan. After gastrulation occurs, the procedure in which the embryo forms a 3-layered structure, the embryo begins to undergo the process of neurulation, which initiates the formation of the nervous organisation. The showtime structure created during neurulation is the neural plate, a thickened area of ectodermal tissue, which will get on to form the neural tube at approximately embryonic day twenty to 27. During the formation and growth of the neural tube, both the rostral and caudal ends of the tube close between embryonic days 25 to 27 to grade a closed-off organisation that will develop into the structures of the central nervous organisation.[8]

Just prior to neural tube closure, the neural tube begins to grow outward at various regions to grade 3 distinct pouches or the primary brain vesicles. From rostral to caudal, the three primary brain vesicles are the prosencephalon, the mesencephalon, and the rhombencephalon. After the formation of the principal brain vesicles, there are farther subdivisions into the secondary v brain vesicles that go on to grade the singled-out structures of the mature central nervous system. The prosencephalon, the precursor to the forebrain, subdivides into the telencephalon and the diencephalon. The mesencephalon does not undergo a further subdivision and gives ascension to the midbrain. The rhombencephalon subdivides into the metencephalon, which goes on to form the pons and cerebellum, and the myelencephalon, which forms the medulla. The reticular germination extends from the medulla up to the region of the brainstem caudal to the diencephalon, thus arising from regions of the mesencephalon, metencephalon, and myelencephalon.[viii]

Blood Supply and Lymphatics

There is a profuse blood supply to the reticular formation due to the lengthened and expansive location of the network of brainstem nuclei and neurons. Blood supply to the brainstem, and thus, to the reticular formation, originates from the vertebrobasilar organization or posterior apportionment of the brain. The beginning of the posterior brain circulation system arises from the vertebral arteries, branches of the subclavian arteries. The vertebral arteries accept a superior grade towards the brain through the transverse foramen of the cervical vertebra. As the vertebral arteries then travel into the dural space, in an anteromedial direction through the foramen magnum of the skull, they unite to class a unmarried basilar artery. Earlier the marriage of the vertebral arteries, the posterior inferior cerebellar artery, as well equally the anterior spinal artery, ascend, supplying blood flow to the inferior cerebellar hemispheres bilaterally, the cerebellar vermis and tonsils, the lateral medulla oblongata, and the upper cervical spinal cord.

After the union of the vertebral arteries, the basilar artery continues a superior class in front of the medulla and pons. It volition afterwards bifurcate at the junction of the pons and mesencephalon to requite rise to the posterior cerebral arteries, supplying the occipital cortex as part of the posterior encephalon circulatory system. Prior to the division into the posterior cerebral arteries, the basilar artery gives off the anterior inferior cerebellar arteries, the pontine perforating branches, and the superior cerebellar arteries. The basilar artery and its subsequent branches supply the rest of the brainstem, including the medulla and pons, the midbrain, and superior structures such as the thalamus, posterior internal capsule, the middle and upper cerebellum as well as the cerebellar vermis.[9]

Clinical Significance

Hypersomnia and Blackout

The reticular activating organisation is one of the major contributors to arousal and consciousness. A devastating consequence of increased intracranial pressure from numerous etiologies is the herniation of encephalon tissue inferiorly to shrink brainstem structures. The degree of herniation determines the severity of bear on on the arousal function of the reticular activating system, ranging from hypersomnolence to coma and potentially death. Hypersomnia is a common issue mail-stroke, and presentation correlates with stroke patients who have infarcts in the thalamus, hypothalamus, and pons. Other disturbances of the ascending reticular activating system, such every bit patients with narcolepsy post mild TBI and spontaneous subarachnoid hemorrhage, besides showed hypersomnia as one of the associated symptoms.[10]

Schizophrenia

Many symptoms of schizophrenia, peculiarly the positive symptoms, such equally hallucinations, sensory gating abnormalities, and sleep-wake disturbances, which are hallmarks of the disease, are idea to exist due to reticular activating arrangement abnormalities. The sleep-wake disturbances that many patients with schizophrenia experience are reductions of slow-moving ridge sleep duration and a decrease in REM latency. At that place is as well speculation that hallucinations may be REM intrusion into a waking state, causing these visual and auditory phenomena. Mail-mortem analyses found that patients with schizophrenia had a greater than sixty% increase in the number of neurons in the pedunculopontine nucleus, part of the reticular formation in the posterior midbrain, compared to patients without the disorder. The pedunculopontine nucleus typically sends excitatory projections to the substantia nigra, which in turn sends dopaminergic projections to diverse regions of the striatum. The pregnant increase in cholinergic neurons in the pedunculopontine nucleus may explain the sleep-wake disturbances since the cholinergic output component of the reticular activating organisation would be increased. The increase in cholinergic neurons in the pedunculopontine nucleus could also lead to an increase in the excitation of the substantia nigra, leading to excess dopaminergic output from that system. The thought is that this increment in neuronal number in the pedunculopontine nucleus is due to the failure of appropriately programmed cell death during nervous system development.[11][12]

Post-Traumatic Stress Disorder

Individuals with Mail-Traumatic Stress Disorder (PTSD) often feel many symptoms related to hyperarousal, flashbacks, anxiety, and disturbances in sleep-wake cycles. Patients with PTSD experience an exaggerated startle response, often to non-harmful auditory stimuli, a phenomenon called sensory gating abnormalities. These patients also have increased REM bulldoze and display many flashbacks and re-experiencing episodes, potentially progressing to hallucinations of past events. A study, including combat veterans with diagnosed PTSD, showed a decreased habituation of the P1 auditory evoked potential, and the caste of decreased habituation was associated with the severity of the patients' flashback symptoms. Individuals who suffered from anxiety disorders comorbid with a diagnosis of PTSD showed a decrease of 50% of the neurons in the locus coeruleus, a role of the reticular activating organization that responds to stress and panic with neurotransmission of norepinephrine. The locus coeruleus normally inhibits the pedunculopontine nucleus. Since patients with anxiety disorders and PTSD showed a meaning reduction in neurons in the locus coeruleus, there may be disinhibition of the pedunculopontine nucleus, resulting in many of the symptoms of PTSD.[11]

Parkinson's Affliction

Parkinson's illness, a progressive neurodegenerative disorder that affects the dopaminergic neurons principally in the substantia nigra, leads to many disruptions in normal movement. These difficulties with movement are displayed by a resting tremor, typically a "pill-rolling" motion of the fingers, progressive stiffness, bradykinesia, cogwheel rigidity, and difficulty initiating or changing movements. In addition to the degeneration of the substantia nigra, individuals with Parkinson's Disease likewise accept locus coeruleus prison cell death. Like to the findings in patients with PTSD, individuals with Parkinson affliction display decreased habituation of the P1 auditory evoked potential, a finding which correlates with the severity of their Parkinsonian symptoms. Enquiry as well plant that the pedunculopontine nucleus is overactive in belatedly-phase Parkinson illness. As the disease progresses, patients typically begin showing decreased habituation of reflexes and symptoms of anxiety and depression, which is a pattern like to PTSD and schizophrenia, as described higher up. Patients with Parkinson disease also report having sleep-wake disturbances and REM sleep behavior disorders common in patients with Parkinson disease. The loss of locus coeruleus neurons and the subsequent disinhibition of the pedunculopontine nucleus may explicate many arousal and motor symptoms present in Parkinson affliction.[11] Individuals who had both poor postural control and sleep disruptions demonstrated longer duration of anticipatory postural adjustments during the initiation of gait and decreased functional activeness betwixt the pedunculopontine nucleus and the supplementary motor area in the locomotor network.[13] In another report of REM behavior disorder and Parkinson disease, smaller volumes of the pontomesencephalic tegmentum, medullary reticular formation, hypothalamus, thalamus, putamen, amygdala, and inductive cingulate cortex were noted in patients with Parkinson illness. This reduction in book coupled with creature studies that demonstrated that lesions in the medullary reticular germination are associated with loss of REM muscle paralysis and the development of REM Behavior Disorder points to dysfunction of the reticular activating arrangement every bit existence an integral component in the development of this disorder.[xiv] Past understanding how the reticular formation plays a function in the pathogenesis of both motor and sleep-wake dysfunction in Parkinson affliction, the greater the number of treatment targets can exist researched and implemented. Currently, experimental deep encephalon stimulation devices targeting the pedunculopontine nucleus are in research for improving axial motor deficits such equally gait freezing and falling that is associated with the progression of Parkinson affliction.[15]

REM Behavior Disorder

REM Beliefs Disorder is a sleep disorder characterized by the patient acting out brilliant, unpleasant, and often fierce dreams. Unremarkably during REM slumber, individuals cannot enact dreams due to muscle paralysis. In patients with REM Behavior Disorder, enquiry showed a greater than 75% reduction in the number of neurons in the locus coeruleus. This reduction in neurons leads to a disinhibited pedunculopontine nucleus, which may offer insight as to why these patients tin act out dreams. Approximately 40% of patients with REM beliefs disorder receive a diagnosis with Parkinson disease ten years after the initial diagnosis of REM behavior disorder. [11]

Narcolepsy

Disorders of the reticular activating system have implications in the pathophysiology of narcolepsy. The hallmarks of narcolepsy are the presence of excessive daytime sleepiness, fragmented slumber, and cataplexy, which is the phenomenon of frequent sleep attacks. Patients also often describe having sleep paralysis, hypnagogic or hypnopompic hallucinations, and nocturnal dyssomnia. The thinking is that the dysregulation of hypocretin/orexin signaling contributes to a large portion of cases of narcolepsy.[16] In 1 report, patients with narcolepsy had significantly decreased, or completely absent P1 auditory evoked potential. Symptoms of narcolepsy may be due to the decreased output of the reticular activating system, potentially the pedunculopontine nucleus in specific.[11] Some other report demonstrated that lesions in the pedunculopontine/laterodorsal tegmental nuclei crusade decreased output and loss of specific orexin peptides, potentially explaining the excessive daytime sleepiness that patients with narcolepsy experience.[2] There have also been studies using quantitative MRI comparing brainstem structures of patients with narcolepsy to healthy participants. These studies found that at that place is a significantly lower R2 relaxation rate in the rostral reticular formation near the superior cerebellar peduncle in patients with narcolepsy. R2 relaxation rates are sensitive for metallic ion chelating elements, such as neuromelanin. Given the location of these findings equally well equally the connections made with orexin projections from the hypothalamus, researchers speculate that the area of dysfunction could be the locus coeruleus or another neuromelanin-containing nucleus. This abnormality of the reticular activating arrangement may explicate the mechanisms of slumber disturbances in narcolepsy.[16]

Spinal Cord Injury

Individuals who suffer from transverse injury to the spinal cord have dysfunction related to the longitudinal tracts relaying data to and from the cerebral cortices. Spinal string injuries have the potential of damaging the reticular formation if they localize to the brainstem. If they practice non straight injure the reticular germination, they disrupt the connection and thus the modulation between the reticular formation and the spinal motor neurons. The traditional signs of upper motor neuron injury, such every bit hyperreflexia and hypertonia, tin exist explained by this dysregulation between the reticular formation and motor neurons. Due to the lack of effective advice between the reticular formation and the spinal cord, the muscles below the spinal cord injury reflexively contract in response to peripheral stimuli due to spinal reflexes. Since there is no modulation and inhibition of contraction by the reticular germination, muscles inappropriately experience increased tone and spasticity. Individuals who have a spinal cord injury also have difficulties with autonomic functions, such equally neurogenic float and dysfunction of the cardiorespiratory system.[ii]

Developmental Influences

Both preterm birth and prenatal exposure to cigarette smoking take correlations with abnormalities of the reticular formation. Individuals who are born preterm demonstrate disruptions of the pre-attentional, attentional, and cortical projections of the reticular activating system throughout their development into childhood and boyhood. Symptoms associated with abnormalities in arousal, difficulties with sleep-wake patterns, and delays in reaction time normally present. Fetuses exposed to cigarette fume demonstrate lasting deficits in arousal, attention, as well equally many cognitive deficits, which may be explained by the presence of nicotinic receptors on neurons in the pedunculopontine nucleus, leading to hyperpolarization-activated cation currents. These deficits may lead to lasting attentional dysfunction later in life.[2] Some other association with development and the reticular activating organization is nowadays in Sudden Infant Death Syndrome (SIDS). Post-mortem assay of patients who expired due to SIDS demonstrated an abnormally big number of dendritic spines in the medullary reticular formation. Ordinarily, the top number of dendritic spines in this region of the reticular germination occurs at 34 to 36 weeks of gestation, and dendritic spines quickly subtract in number after this peak. Researchers hypothesize that this persistence of dendritic spines demonstrates incomplete development of the reticular activating system, potentially leading to dysfunction in college levels of respiratory control, contributing to the pathophysiology of SIDS.[17]

Review Questions

Effigy

Reticular activating system. Prototype courtesy S Bhimji MD

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Source: https://www.ncbi.nlm.nih.gov/books/NBK556102/

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