Neuroanatomy 2 PDF

UMN/LMN + Proprioception + Nociception Sign in even if you’re looking at this later :) Cyrus Salvani Upper Motor Neurons (UMNs) + Lower Motor Neurons (LMNs) Upper vs Lower Motor Neurons Both are Descending Efferent Motor Pathways Upper Mot...

UMN/LMN + Proprioception + Nociception Sign in even if you’re looking at this later :) Cyrus Salvani Upper Motor Neurons (UMNs) + Lower Motor Neurons (LMNs) Upper vs Lower Motor Neurons Both are Descending Efferent Motor Pathways Upper Motor Neurons (UMNs) Cell Bodies in the Brainstem Initiate voluntary muscle action Axons synapse w/ LMNs Influence LMN activity Lower Motor Neurons (LMNs) Cell Bodies in the Ventral Horn Innervate muscles UMN axon travel via Dorsolateral Motor System or Ventromedial Motor System UMN Pathways Have Somatotopy Somatotopy = point-for-point correspondence of function to location in the CNS LMN axons travel to skeletal muscle through peripheral nerves Can be stimulate by Conscious Effort (UMN) or Reflexes (Peripheral Afferent) Dorsolateral Motor System Function = Precise fractionated movements Target = Distal Limb, Flexors more than Extensors Lesion = Decreased / Absent voluntary fine motor movement caudal to site of lesion Ventromedial Motor System Function = Posture / Balance + Whole Limb Movements Target = Proximal Limb, Extensors more than Flexors Lesion = Decreased / Absent voluntary whole limb movement caudal to site of lesion UMN + LMN Signs Upper Motor Neuron Signs Lower Motor Neuron Signs Paresis to Paralysis // Spastic Paralysis Paresis to Paralysis // Flaccid Paralysis Normal to Increased muscle tone Decreased to Absent muscle tone Normal to Increased spinal reflexes Decreased to Absent spinal reflexes Clonus Rapid-onset muscle atrophy Slow muscle atrophy  Site of Injury Thoracic Limb Deficit Pelvic Limb Deficit C1 - C5 UMN UMN C6 - T2 LMN UMN Cervicothoracic Intumescence T3 - L3 Normal UMN L4 - S2 Normal LMN Lumbosacral Intumescence Lesions directly at either intumescence will present with LMN signs of the respective limb Lesions will cause UMN signs caudal to the site of the lesion Urinary Continence Urethra: Pudendal Nerve (S1 - S3) Afferent + Efferent fibers Voluntary control of micturition via urethralis m Reflex closure of urethralis m. at external urethral sphincter Urinary Bladder: Pelvic Nerve (S1 - S3) Parasympathetic Sensory to stretch of bladder wall Autonomic contraction of Detrusor m. >> Urinary bladder emptying Hypogastric Nerve (Lumbar NN) Sympathetic Inhibits Detrusor m. action >> Allows urinary bladder filling Bladder Storage Urine filling stretches bladder wall Visceral afferents via pelvic n Animal is aware of need to urinate Some urine enters urethra Somatic afferent via pudendal n Animal aware it needs to urinate Reflex contraction of urethralis m via pudendal n Voluntary control of urethralis m via pudendal n Sympathetic inhibition of detrusor m via hypogastric n Allows urinary bladder filling Micturition Animal knows it need to pee via pudendal + pelvic nn Conscious voluntary relaxation of urethralis m Parasympathetic contraction of detrusor m via pelvic n Incontinence = Lesions In Spinal Cord Innervating the Bladder Urinary Bladder is innervated by S1 - S3 UMN Signs observed in lesions cranial to S1 -S3 LMN Signs observed in lesions at S1 - S3 UMN Bladder Signs LMN Bladder Signs Hypogastric N intact = Normal SNS control Continuously leaking piss Normal inhibition of detrusor m = fills normally No voluntary control // No tone in urethralis m No reflex constriction of urethralis m Increased urethralis m tone = constant constriction Bladder stays flaccid since it’s not filling Pelvic N abnormal = abnormal PSNS control Unable to contract detrusor m Bladder fills with urine but urethralis m is still constricted Bladder fills too much and overloads urethralis m >> Inconsistent urine leakage Resistance to manual expression due to urethralis m Proprioception Proprioception = Perception of one’s own body position in space Receptors: Golgi Tendon Organs = Joints / Tendons Muscles Spindles = Muscle length Skin Mechanoreceptors = Tactile sensation Postural Reaction Tests (while standing) for conscious proprioceptive (CP) deficits  Conscious Proprioception: General Somatic Afferents (GSA) Parietal Lobe - Somatosensory Cortex Brain integrates afferent information to provide perception of body in space >> conscious proprioception Two Pathways: Dorsal Column of the Medial Lemniscus (DCML) Ascending CP information about limbs + body Trigeminal Pathway Ascending CP information about the face Can’t accurately test in domestic animals Proprioception Testing During Locomotion : Ataxia While Standing: Postural Reaction Tests (PRTs) Look for gait abnormalities (Neurological Specific for CP function Ataxia) Abnormal PRTs = CP deficits Wide swing phase >> Now need to locate the lesion Hypermetria Longer Stride Knucking/dragging feet Not always definitive signs of proprioception Ataxia is NOT specific to CP deficits Conscious Proprioception (CP) deficits - when a patient fails a proprioceptive test  Placing w/ + w/out vision Knuckling (Proprioceptive Hemistanding Positioning) Postural Reaction Tests Hopping Wheelbarrowing DCML Pathway Receptors = Proprioceptors Skin mechanoreceptors Muscle Spindles = Detects length (stretch) Golgi Tendon Organ = Detects tension Afferent cell bodies in Dorsal Root Ganglia Δ Afferent fibers ipsilaterally ascend DCML Decussation at brain stem: Medulla Contralateral thalamus relays information via Internal Capsule Afferent information reaches contralateral Somatosensory Cortex DCML axons = large + heavily myelinated >> Vulnerable to compression Superficial spinal cord lesion may cause CP deficits Fasciculus Gracilis = Pelvic Limb Fasciculus Cuneatus = Thoracic Limb What if there's ataxia but no CP deficits? Vestibular Ataxia Lesion in Vestibular Apparatus // Vestibulocochlear Nerve (CN VIII) CS: Resting Nystagmus + Head Tilt + Leaning + Falling/Rolling Ataxic but NO CP deficits Cerebellar Ataxia Cerebellum = Rate + Range + Force CS: Wide Stance + Intention Tremors + Truncal Sway + Exaggerated response to PRT + Absent Menace + Normal Mentation Ataxic but NO CP deficits Pass PRTs but look weird doing it lol Neurological Gait (Ataxia): Proprioceptive Ataxia Vestibular Ataxia Cerebellar Ataxia Trigeminal Pathway CP from the face + oral cavity Afferent= Trigeminal Nerve (CN V) Still decussates at brain stem Travels to Contralateral thalamus Destination = Somatosensory Cortex All proprioceptive tracts decussate at the brainstem to reach the contralateral thalamus Therefore, all proprioceptive tracts from one side of body will reach the contralateral somatosensory cortex // parietal lobe Nociception = Perception of noxious stimuli Receptors + Stimuli Receptors = Nociceptors Simulus = Mechanical + Thermal + Chemical (2) Nerve Types Aδ (Delta) Fibers - Rapid Response Fast conducting, myelinated C Fibers - Slow Long Lasting Response Sow conducting , unmyelinated Distribution in the body Superficial Somatic Structures: 1 Aδ : 2 C Visceral Structures: 1 Aδ : 10 C Pain is a Response Nociception = afferent component of withdrawal reflex + pain response It is possible to have intact pain response with absent withdrawal reflex Efferent motor neuron may have a lesion Test until you see a BEHAVIORAL Response Turning head toward stimulus Biting Vocalization Attempt to escape Changes in respiratory + heart rate does NOT imply cortical involvement >> These are made in the brainstem not the cortex Ascending Nociceptive Pathways General Visceral Afferent (GVA) = More C Fibers Large overlapping receptor fields >> poorly localized Receptors to stretch, ischemia, dilation, spasm, inflammation General Somatic Afferent (GSA )= More Aδ Fibers Discriminate “sharp” pain Spinocervicothalamic Tract = Superficial Pain Highly Discriminate = Hella Somatotopy Stimuli can be precisely located More susceptible to compressive injury than Spinoreticular Tract Stimulus = LIGHT pinch >> Don’t wanna stimulate deep pain Primary Afferent in Dorsal Horn Secondary Afferent (Interneurons) mediate local reflex Interneurons also project fibers cranially in IPSILATERAL tract in dorsal portion of Lateral Funiculus Fibers ascend spinal cord and decussate in brain stem Fibers reach contralateral thalamus Thalamus > Internal Capsule > Cortex Spinocervicothalamic Tract = Superficial Pain Spinoreticulothalamic Tract = Deep Pain Indiscriminate = Somatotopy not well defined Patient experiences pain but can’t specifically identify source Pathway is multi-synaptic + diffuse Recruits as many things as possible to transmit signal to brain More centrally located w/in spinal cord than superficial pain tract Loss of deep pain is a poor prognostic indicator Must stimulate an area with a lot of C nociceptors Stimulus = Apply hemostats to base of toenail >> Do NOT include the skin (will also stimulate superficial tract) Primary Afferent in Dorsal Horn Secondary Afferent (Interneuron) diffuse the signal a.k.a sends the signal absolutely everywhere >> Sends stimulation to adjacent spinal cord segments + ALL Funiculi Bilateral axonal fibers are decussating to basically cover all the white matter of the spinal cord Reticular Formation in brain stem Multiple cortical + subcortical destinations >> Activation of limbic system = emotional response to pain Spinoreticulothalamic Tract = Deep Pain Head Nociception = Trigeminal Nerve (CN V) All three divisions of CNV receive sensation of touch and pain Transmit afferent fibers to Trigeminal Ganglion Pain Modulation Multimodal Pain Control = Using a combination of different avenues to decrease pain in the patient Changes in Cortical Perception: Hypoalgesia = Decreased perception of pain Analgesia = Complete absence of pain perception Anesthesia = Absence of all sensory perception Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) = Hypoalgesic Drugs Injured tissues release inflammatory mediators eg prostaglandins / leukotrienes Directly stimulate nociceptors + Lower threshold of nociceptors NSAIDs stop formation of prostaglandins Opioids // Narcotics = Hypoalgesic Drugs Bind opiate receptors in brain / spinal cord / peripheral nerves Eg Morphine, Codeine, Fentanyl, Hydromorphone Local Anesthetic // Nerve Block = Administered Analgesics Inhibits nociceptors Alter rate of depolarization and repolarization of excitable membranes Eg Carbocaine, Lidocaine, Bupivacaine Descending Modulatory Pathways Neurotransmitters at level of spinal cord can have antinociceptive properties Decrease pain transmission + perception Eg Endorphins, Serotonin, Norepinephrine Anxiety / Fear can amplify pain perception >> Stress reduction can help reduce pain perception Questions??