Motor and Sensory Pathways Lecture 19 PDF

Motor and sensory pathways – NAS Lecture 19 – 01/12/2023 Motor pathways Innervation of skeletal muscle is achieved via the integration of upper and lower motor neurones. ​ Upper motor neurones – originate from the cerebral cortex. ​ Lower motor neurones – originate from the ventral horn of th...

Motor and sensory pathways – NAS Lecture 19 – 01/12/2023 Motor pathways Innervation of skeletal muscle is achieved via the integration of upper and lower motor neurones. ​ Upper motor neurones – originate from the cerebral cortex. ​ Lower motor neurones – originate from the ventral horn of the spinal cord, or from cranial nerve nuclei. Axons of upper motor neurones must therefore synapse with the lower motor neurones, or with interneurons that connect to LMNs. To do this, they must follow a pathway from the cerebral cortex to the spinal cord. Motor homunculus A motor homunculus helps to show the targets of different regions within the primary motor cortex of the cerebral cortex. Role of the cerebellum The cerebellum is responsible for the coordination of movement. It does so by combining motor input from the motor cortex of the brain with proprioceptor sensory input (input on position, speed and movement of limbs). By doing so, it can feedback to the motor cortex via the thalamus, providing co-ordination to the movement. Corticospinal/pyramidal tract This is the neuronal pathway that extends from the brain to the spinal cord. 1.​ Origin Cell bodies of upper motor neurones are found in the primary motor cortex, secondary motor cortex and a small part of the somatosensory cortex.​ 2.​ Pathway to brainstem The axons of these UMNs travel to the brainstem, passing through the corona radiata and the internal capsule. At the medulla of the brainstem, the descending axons form a visible ridge known as a pyramid on the surface of the medulla. For this reason, the pathway is also known as the pyramidal pathway or tract.​ 3.​ Decussation of pyramids and descent down spinal cord At the pyramid, most of the fibres from one side of the cerebral cortex usually cross over to the other side. This is known as decussation of the pyramids. This means that skeletal muscle of the right side of the body would be controlled by the left cerebral cortex, and vice-versa. Lateral corticospinal tract Around 85-90% of corticospinal fibres decussate. In doing so, they descend the spinal cord as the lateral corticospinal tract, before synapsing with either interneurons or directly with lower motor neurones. The lateral corticospinal tract is responsible for fine, skilled voluntary movements, such as finger movement. It also influences important reflex arcs which control the movement of the distal ends of limbs (e.g. fingers, toes). ​ Medial/ventral corticospinal tract Around 10-15% of corticospinal fibres do not decussate. They continue down the spinal cord medially and ventrally. This ventral corticospinal tract controls axial muscles (muscles of the trunk and head). It usually involves bilateral contraction of muscles (contraction on both sides of body), for functions such as posture control and swallowing. Corticobulbar tract This is the pathway that extends from the cerebral cortex to cranial nerve nuclei in the brain. It is therefore responsible for the activation of skeletal muscles of the head and neck, by synapsing with lower motor neurones. 1.​ Origin – Same as corticospinal tract, originates from primary and secondary motor cortexes and a small part of the somatosensory cortex.​ 2.​ Pathway to cranial nerve nuclei The axons of the upper motor neurones of this pathway travel along the corona radiata and internal capsule to reach the brainstem. This is where the motor cranial nerve nuclei are located, for cranial nerves III, IV, V, VI, VII, IX, X, XI and XII.​ 3.​ Synapsing At the cranial nerve nuclei, the UMNs synapse with LMNs. The LMNs then innervate the skeletal muscles of the corresponding cranial nerve (e.g. facial muscles, mastication muscles). Extrapyramidal tracts These are tracts which do not originate from the motor cortexes, but rather they originate from other parts of the brain, such as vestibular nuclei, reticular nuclei, and basal ganglia. They control movement, posture, and muscle tone. ​ Vestibular nuclei – influence spinal motor neurones via the descending vestibulospinal tract.​ ​ Reticular nuclei – influence spinal motor neurones via the descending reticulospinal tract. ​ ​ Basal ganglia - influence lower motor neurones of the brainstem and spinal cord. They inhibit involuntary or inappropriate movements. Parkinson's disease This is a disorder of the basal ganglia caused by dopamine deficiency. Treated via medication, exercise and therapies. It leads to symptoms such as: ​ Akinesia – inability to move voluntary muscles. ​ Muscular rigidity ​ Bradykinesia – very slow movements of voluntary muscles. ​ Festinating gait – rapid, small steps during walking to maintain balance, countering involuntary leaning forwards of the trunk. Motor neurone lesions Upper motor neurone lesions – lead to increased muscular tone, hyperreflexia, muscle spasticity and rigidity. Lower motor neurone lesions – lead to hyporeflexia or areflexia, reduced muscle tone, fasciculations and finally muscle atrophy. One way to help differentiate between an LMN and UMN lesion is the Babinsky reflex, which occurs after the sole of the foot is stroked. It is naturally present in children but disappears in adulthood. ​ +ve sign – big toe moves upward, other toes fan out. This is a sign of a UMN lesion. ​ -ve sign – Downward flexion of toes. This is not a UMN lesion. If other LMN lesion symptoms are present, it is likely to be an LMN lesion. Sensory pathways Somatosensory homunculus Sensory pathways in the spinal cord Sensory information from a peripheral region of the body (not the head) reaches the somatosensory cortex via a sequence of 3 sensory neurones: ​ First-order neurones – from receptor to second-order neurone. Cell body in the dorsal root ganglion. First order neurones mainly use glutamate as neurotransmitter.​ ​ Second-order neurones – Cell body in the dorsal horn or medulla oblongata (depending on pathway). Axons ascend the spinal cord and synapse with third-order neurones in the ventral posterior (VP) nucleus of the thalamus.​ ​ Third-order neurones – Cell body in the thalamus. Receive info from second-order neurones. Extend axons which terminate at the primary somatosensory cortex. There are 3 main pathways through which sensory afferent input from peripheral receptors reaches the somatosensory cortex through the spinal cord. ​ Dorsal column pathway ​ Spinothalamic tract ​ Spinocerebellar tract Dorsal column pathway This pathway delivers sensory input of discriminative touch (fine touch e.g. pressure or vibration) and proprioception.  1)​ First-order afferents deliver sensory information from receptors (such as Meissner and Pacinian corpuscles, Ruffini endings, muscle spindles and Golgi tendon organs), through the dorsal root ganglion, and the axon extends into the grey matter of the spinal cord. ​ 2)​ The axon then ascends the spinal cord as two bundles on either side of the spinal cord:​ Fasciculus gracilis – bundle of axons giving input from lower limb and trunk on that side of the body.​ Fasciculus cuneatus – bundle of axons giving input from upper limbs and trunk on that side of the body.​ 3)​ The fasciculus gracilis terminates at the nucleus gracilis of the medulla oblongata. This is where it synapses with second-order neurones.​ The fasciculus cuneatus terminates at the nucleus cuneatus.​ 4)​ Second-order axons then ascend to the tegmentum of the medulla oblongata, where they decussate to the other side (sensory decussation).​ 5)​ The axons ascend together as the medial lemniscus.​ 6)​ The axons terminate at the VP nucleus of the thalamus, where they synapse with third-order neurones. ​ 7)​ Third-order axons extend from the thalamus to the somatosensory cortex (Brodmann areas 1, 2 and 3). Spinothalamic tract This pathway delivers sensory input of pain, temperature, crude touch (light touch) and pressure. 1)​ First-order afferents deliver sensory information from receptors, through the dorsal root ganglion, and the axon extends into the grey matter of the spinal cord.​ 2)​ The axon synapses with second-order neurones. ​  3)​ The second-order afferents cross the midline of the spinal cord and extend to the other side.​ 4)​ Second-order afferents ascend the spinal cord towards the thalamus, passing through the medulla oblongata and midbrain. ​ 5)​ At the thalamus, in the VP nucleus, the second-order axons synapse with third-order neurones.​ 6)​ Third-order axons extend to the somatosensory cortex (Brodmann areas 1, 2 and 3). ​ Spinocerebellar tracts There are 4 ascending sensory tracts which deliver information to the cerebellum. ​ Dorsal spinocerebellar tract – for unconscious proprioception from muscle spindles and Golgi tendon organs.​ ​ Cuneocerebellar tract - for unconscious proprioception from muscle spindles and Golgi tendon organs.​ ​ Ventral spinocerebellar tract – for monitoring the state of spinal reflex arcs in the lower limbs.​ ​ Rostral spinocerebellar tract - for monitoring the state of spinal reflex arcs in the upper limbs. Trigeminothalamic tracts Sensory input from afferent axons within cranial nerves reaches the somatosensory cortex via this pathway. 1)​ First-order axons carrying sensory information (e.g. pain, temperature, touch, proprioception) from receptors travel to nuclei in the brainstem where they synapse.​ The nuclei include the mesencephalic nucleus (proprioception), chief sensory nucleus (touch, pressure) and spinal nucleus (pain, temperature)..​ 2)​ From the nuclei, axons of second-order neurones extend to the thalamus, where they synapse with third-order nuclei.​  3)​ Third-order axons deliver the information to the somatosensory cortex. Brown-Sequard syndrome This syndrome occurs when there is a hemi-lesion in the spinal cord (spinal cord is damaged on one side). As a result of the damage to the spinal cord, both the motor and sensory pathways will be disrupted. Effect on motor pathway: ​ Upper motor neurone signs occur only on the same side of the lesion, such as muscle weakness and hemiplegia (paralysis on one side only), affecting muscles below the level of the lesion. ​ Lower motor neurone signs may occur on the same side, in muscles at the vertical level of the lesion itself due to damage to lower motor neurones. Effect on sensory pathways: ​ Proprioception and touch are lost at the side of the lesion. ​ This is because these senses are carried by the dorsal column pathway, where the tract remains in the same side and only decussates (crosses to the other side) at the medulla.​ ​ Pain and temperature sensation are lost on the opposite side to the lesion.​ This is because these senses are carried by the spinothalamic tract which decussates at the level of the second-order neurone