Anatomy of the Spinal Cord PDF
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This document provides an overview of the anatomy of the spinal cord, including its location, composition, and key structures. It also touches upon pain pathways and types of nerves in the body. The document likely serves as educational material for students studying biology or human anatomy.
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Anatomy of the Spinal Cord Located within the vertebral canal, extending from the brain stem. Receives information from and controls the trunk and limbs. Composed of 31 pairs of spinal nerves. Ends at the L1/L2 intervertebral disc, a point of significance for medical...
Anatomy of the Spinal Cord Located within the vertebral canal, extending from the brain stem. Receives information from and controls the trunk and limbs. Composed of 31 pairs of spinal nerves. Ends at the L1/L2 intervertebral disc, a point of significance for medical conditions. it is in cylindrical shape Central canal H shaped – separation of cell bodies from nerve fibres Dorsal root – afferent fibres (conducts signals towards the CNS) Ventral root – efferent fibres – conducts signals away from CNS Key Structures Intervertebral foramina allow nerves to exit the spinal column. Cauda equina consists of lumbar and sacral nerves; a collection of nerve roots below the spinal cord. Spinal nerved end at L1/L2 DISC – development speed – vertebral column grows faster than spinal cord, so after L1 AND L2 corresponding nerves do not exit the vertebrate Cauda equine syndrome https://www.pinterest.com/pin/432556739200491284/ http://pennstatehershey.adam.com/content.aspx?productId=114&pid=28&gid=000415 Picture: https://www.quora.com/Why-does-our-left-hemisphere-of-brain-control-our-right-side-of-our-body-and-the-right-our-left However……... - The olfactory system isn’t reversed at all. - The visual system is only partly reversed; each eye sends some information to each side of the brain. - Sounds are analysed on both sides of the lower portions of the brain but on only one side of the cortex. https://www.quora.com/Does-olfactory-nerve-have-a-ganglion https://www.pinterest.com/pin/75083518765722309/ Spinothalamic tract Spinocerebellar tract and Dorsal columns Corticospinal tract Picture: http://vanat.cvm.umn.edu/neurLab2/pages/SpThalTract.html Picture: http://resizeme.club/picresize-212_12.html These are longitudinal running nerve fibres Spinothalamic trat – gets information the muscle and joint receptor, sensory tract, carried nociceptive (special nerve endings under the skin), temperature, crude touch, and pressure from the skin to the thalamus (when we get injured we release prostaglandins) Spinocerebellar tract and Dorsal columns – Fine touch and proprioception [Ascending tracts from trunk to brain] Corticospinal tract – Skilled voluntary movement – Majority of Upper Motor Neurons within this tract. Signals from the cerebral cortex to the spinal cord. [Descending tracts from brain to trunk] How do we feel pain? Chemical released from the injury activates nociceptors – this releases substance P and glutamate (pain producing neurotransmitters) Prostaglandins get released due to inflammatory response and activated the nociceptors Alpha Beta Fibres Alpha-delta (aδ) fibres C-fibres (Visceral Pain) (Touch) (Somatic Pain) Large, mylelinated and fastest Small myelinated fibres which Smalleat diameter. Non- conducting conduct rapidly myelinated fibres with low conduction velocity Carry information related to Sharp Pain Diffuse pain touch/pressure Precisely located Precisely located Not distinctly localised Neurons project with a peripheral axon to target tissue and central axon to the spinal cord There are 3 classes of afferent fibres: There are two types of nociceptive pain: Somatic pain has an external cause and is transmitted by the alpha fibres. Activation of the nociceptor in skin and skeletal muscle patient can normally identify exactly where the pain. It can be reproduced by touching ot moving the area or tissue involved Visceral pain has an internal cause and is transmitted through the C fibres. Activation of the nociceptor in the thoracic or abdominal organs is often poorly localised and can feel like a vague deep ache Pain Transmission Pathway Involves three orders of neurons: o 1st Order Neuron: Cell bodies in the dorsal root ganglion, relaying information from the periphery. o 2nd Order Neuron: Follows the spinothalamic tract and synapses in the thalamus. o 3rd Order Neuron: Sends signals to the somatosensory cortex, determining pain location. Types of Pain Fibers Alpha Beta Fibers: Large, myelinated, fast-conducting fibers for touch/pressure. Alpha-delta (aδ) Fibers: Small myelinated fibers for sharp, localized pain. C-fibers: Non-myelinated, slower fibers for diffuse, visceral pain. Descending Pain Pathway Inhibits pain perception via the periaqueductal grey matter (PAG). Involves serotonergic and noradrenergic neurons to modulate nociceptive neurotransmitters. Serotonin descends to the dorsal horn of the spinal cord and forms excitatory connections with inhibitory interneurons Enkephalins and dynorphins are released to bind with mu-opioid receptors, reducing pain sensation. Descending pathway activated by somatosensory cortex It responds to and inhibits the ascending pathway to mitigate pain sensation. Natural opioids: enkephalins, endorphins and dinorphins Chemical Receptor sites at axon terminals Serotonin and Noradrenaline- involved in this system. Activation of Serotonergic (5-HT) and Noradrenergic (NA) neurons to prevent nociceptive neurotransmitters Upper and Lower Motor Neurons (UMN & LMN) UMN: Transmit signals from the brain to the brainstem and spinal cord, with a majority crossing at the medulla; involved in voluntary movement initiation. LMN: Transmit signals from the spinal cord to muscles; responsible for muscle contraction. UPPER MOTOR Neurons – located in cerebral cortex of the brain and facilitate the transmission of signals from the brain to the brain stem and spinal cord nerves (UMN) and then on to the skeletal muscles (LMN) – the target organ for the motor neurons. Descending motor pathways that control activity of LMN (Signals from UMN required to activate LMN’s) Corticospinal (pyramidal) and corticobulbar pathways important Breakdown leads to: loss of individual movement of digits, Reduced extension and abduction of upper limbs, Reduced flexion of lower limbs (referred to as Pyramidal weakness) PYRAMIDAL system = voluntary motor movement Communication between upper and lower motor neurons occur in the vertebrae LOWER MOTOR Neurons – located in spinal cord and their terminal extend all the was to muscle fibres and tendons. Skeletal muscle contraction is initiated by LOWER motor neurons Arise in brain stem (forming the cranial nerves) and those leaving the ventral horns of the spinal cord (SPINAL NERVES). LMM innervate muscle on same side of the body (effects of lesions are ipsilateral to the lesion) DAMAGE TO LMM à paralysis (loss of movement, or paresis (weakness) of the affected muscles Upper Motor Neurones (UMN) Example Want to move RIGHT thumb. UMN arise from the LEFT Primary motor cortex Pass through the internal capsule through the midbrain and brainstem (Medulla and pons) Majority of Neurons cross over to the opposite side of the body at the medulla. Majority of UMN contained within the Lateral corticospinal tract through the spinal cord. Once the UMN reaches the correct vertebral level (via the spinal cord) it will synapse with the LMN at the anterior horn. The LMN will then target the muscle responsible for the movement of that body part (ie the muscles involved in the movement of the right thumb) Upper Motor Neuron Lesions Cause spasticity, weakness, hyperreflexia, and a positive Babinski reflex without muscle wasting. Strength is affected in specific movements but generally maintains bulk. Causes of UMN Lesions Lower Motor Neuron Lesions Result in muscle weakness or paralysis with atrophy, fasciculations, and hyporeflexia. Affects individual muscles, such as in Bell's Palsy. Signs of UMN lesions Signs of UMN lesions – will depend on which side of the lesion is. Little or no muscle atrophy Weakness to muscle Hyperactive deep tendon reflex – reflex is amplified due to UMN not working and not regulating the signals at that level. Diminished or absent superficial reflex – Positive Babinski reflex (scrape sole of foot and het extension and fanning of the toes) Causes of LMN Lesions Signs of LMN lesions Signs of LMN lesions Muscle atrophy (wasting) due to the signals not reaching the muscle therefore not activating the muscle Flaccid paralysis. No plantar response due to no signals reaching the muscle Absent tendon reflexes again due to no signals reaching the muscle Fasciculations – some muscle fibres still receiving some signals but not enough to turn on the whole muscle. Ie bicep would not contract but muscle fibres within the bicep receiving some signs making individual fibres contract (fasciculation) Lower and upper motor neurone lesions Upper motor neurone syndrome Weakness or paralysis of specific movements (ie extension of upper limbs) No wasting of muscles Increased resistance to passive stretching muscles (spasticity) Hyperactivity of deep tendon reflexes (hyperreflexia) Emergence of extensor plantar response (Babinski reflex) Loss of abdominal reflexes Lower motor neurone syndrome Weakness (paresis) or paralysis (plegia) of individual muscles (ie Bells Palsy, Bulbar palsy) Wasting of muscles Fasciculation (of muscles) Reduced resistance to passive stretching (hypotonia) Diminution of loss of deep tendon reflexes (hyporeflexia or areflexia) Causes: CVA, multiple sclerosis, spinal cord injury, acquired brain injury Blood Supply to the Spinal Cord Supplied by anterior and posterior spinal arteries with additional input from radicular arteries. Vulnerable regions include the thoracic area and anterior cord; occlusion can lead to paraplegia and incontinence. Venous Drainage Drains via anterior and posterior spinal veins into an internal vertebral venous plexus. Ascends to lumbar, azygos, and hemiazygos veins. Venous drainage Anterior and posterior spinal vein Via anterior and posterior radicular vein into internal vertebral venous plexus Ascends to: Lumbar veins Azygos Hemiazygos veins Picture: https://neupsykey.com/vasculature-of-the-central-nervous-system/ Ganglions Clusters of nerve cells housing the cell bodies of afferent and efferent nerve fibers. Made up of somata and dendritic structures Facilitate communication between various neurological structures and comprise complex systems known as "plexus." Types include: o Dorsal root ganglia (sensory neurons) o Cranial nerve ganglia (cranial neurons) o Autonomic ganglia (autonomic nerves)