Class 1 – Notes PDF

Class 1 – Notes 2025-01-06 8:20 AM CNS Anatomy: Brain and Spinal cord Spinal cord is connected to the brainstem and runs through the spinal canal Cranial nerves exit the brainstem...

Class 1 – Notes 2025-01-06 8:20 AM CNS Anatomy: Brain and Spinal cord Spinal cord is connected to the brainstem and runs through the spinal canal Cranial nerves exit the brainstem Nerve roots exit the spinal cord Spinal cord carries signals back & fourth between the brain & peripheral nerves Controls most body functions including Awareness Movements Thoughts Speech Memory Major Parts of The Brain: Brain Stem Continuous with spinal cord, contains: Medulla oblongata Pons Midbrain Cerebellum Posterior to brainstem Diencephalon Superior to brain stem, contains: Thalamus Hypothalamus Epithalamus Cerebrum Largest part of brain, sits on diencephalon Cranial Nerves: Nerves that emerge from or enter the skull, as opposed to the spinal nerves which emerge from the vertebral column Cranial nerves come directly from the brain through the skull We have 12 cranial nerves I. Olfactory Smell II. Optic Vision III. Oculomotor Eye movement and pupil reflex IV. Trochlear Eye movement V. Trigeminal Face sensation & chewing VI. Abducens Lateral eye movement VII. Facial Face movement & taste VIII. Vestibulocochlear Hearing & balance IX. Glossopharyngeal Throat sensation, taste, & swallowing X. Vagus Movement, sensation & abdominal organs XI. Accessory Neck movement (trapezius & SCM) XII. Hypoglossal Tongue movement Motor Pathways: The neural circuits or pathways in the nervous system Responsible for transmitting signals from the brain to the muscles, leading to voluntary muscle movements These pathways coordinate and control muscle contractions There are two primary motor pathways 1. The corticospinal pathway 2. The extrapyramidal pathway Together to ensure smooth and coordinated movements Damage or disruptions to these pathways can result in motor impairments such as Weakness, tremors, or difficulties in controlling movements Understanding motor pathways is crucial in the fields of neurology & rehabilitation, as it helps diagnose and treat various motor disorders Two Pathways: 1. Corticospinal Pathway Originates in the primary motor cortex of the brain Consists of upper motor neurons that travel through the internal capsule, brainstem, and spinal cord The upper motor neurons synapse with lower motor neurons in the spinal cord The lower motor neurons then transmit signals to the muscles, causing voluntary muscle contractions Damage or disruptions can cause: Motor deficits, such as weakness, paralysis, or impaired coordination Upper Motor Neurons (UMNs) Originate in the primary motor cortex of the cerebral cortex Travel through the internal capsule, brainstem (particularly the medulla), and spinal cord Lower Motor Neurons (LMNs) Located in the spinal cord Receive signals from the upper motor neurons Extend their axons out of the spinal cord to innervate skeletal muscles Muscle Contraction When the LMN receive signals from the UMN, they transmit electrical impulses to the skeletal muscles This results in the contraction of the targeted muscles, leading to voluntary movements 2. Extrapyramidal Pathway Involves multiple subcortical nuclei and brain regions outside the primary motor cortex Plays a role in coordinating and regulating muscle tone, posture, and involuntary movements Unlike the corticospinal pathway, which directly connects the cortex to the spinal cord, the extrapyramidal pathway involves more complex and indirect connections Spinal Segments: Cervical Spine 7 segments Transmit signals to and from: Head Neck Shoulders Arms hands Thoracic Spine 12 segments Transmits signals to and from: Part of the arms The anterior and posterior chest Abdominal areas Lumbar Spine 5 segments Transmit signals to and from: Legs and feet Some pelvic organs Sacral Segments 5 fused vertebrae Transmit signals to and from Lower back and glutes Pelvic organs Genital areas Some areas in the legs and feet Coccygeal Segment 1 coccygeal remnant Located at the bottom of the spinal cord Dermatomes and Myotomes: Dermatomes An area of skin supplied by sensory fibers from a single spinal nerve These nerves transmit sensory information (such as pain, temp, and touch) from specific areas of the skin to the spinal cord and then to the brain Typically organized in a segmented pattern corresponding to the spinal nerves Myotomes A group of muscles primarily innervated by the motor fibers of a single spinal nerve Motor neurons in the spinal cord send signals to specific muscles through these myotomes, enabling voluntary muscle movement Also organized in a pattern corresponding to specific spinal nerves C1/C2 Neck flexion/extension C3 Neck lateral flexion C4 Shoulder elevation C5 Shoulder abduction C6 Elbow flexion/wrist extension C7 Elbow extension/wrist flexion T1 Finger abduction L2 Hip flexion L3 Knee extension L4 Ankle dorsiflexion L5 Big toe extension S1 Ankle plantarflexion/ankle eversion/hip extension S2 Knee flexion Deep Tendon Reflexes: Why? Quickly confirm the integrity of the spinal cord Differentiate between upper motor nerve lesions (UMNL) and lower motor nerve lesions (LMNL) UMN = increase reflexes LMN = decreased reflexes What are we looking for? Asymmetry: test the opposite side immediately after Threshold for stimulus: how hard? Does it elicit the same response? Hyperactive = CNS lesion – test for weakness, spasticity Hypoactive = PNS, spinal roots, plexus – check for weakness, atrophy, fasciculations Deep Tendon Reflexes Biceps brachii – C5 Brachioradialis – C6 Triceps brachii – C7 Quadriceps – Patellar L4 Gastrocnemius/soleus - Achilles S1 Grading: 0 Absent 1+ Trace 2+ Normal 3+ Brisk 4+ No sustained clonus (very brisk) 5+ Sustained clonus Assessments: Sensory Testing Touch perception – light vs deep Temperature perception – hot vs cold Pain perception Two-point discrimination Proprioception test Vibration sense with a tuning fork Comparisons should be made from one side to the other & from proximal to distal of each extremity Assessment: MMT MMT purposes Baseline for Rx, Dx and injury, set up a rehab program Break test: with gravity, gravity eliminated (plane parallel with gravity), gravity assisted (gravity used to help assist movement, eccentric contractions) Grading for MMT: Grade 5 Normal Able to hold against gravity with max resistance, or to move in to test positions & hold against gracity at max pressure Grade 4 Good As above except with moderate resistance Grade 3 Fair Holding test position or moving in to test position against gravity Grade 2 Poor Moving though the full range with gravity eliminated Grade 1 Trace Mm contraction can be palpated Grade 0 Zero No contraction can be elicited UMN vs. LMN: Upper motor neuron (UMN) lesions and lower motor neuron (LMN) lesions are two distinct types of neurological conditions that affect different parts of the nervous system and result in different patterns of symptoms It's important to note that the terms "upper motor neuron" and "lower motor neuron" refer to specific anatomical pathways and do not encompass all possible conditions Upper Motor Neuron Lesion (UMN): Location Occur within the central nervous system (CNS), specifically within the brain or spinal cord Effect on Muscle Tone UMN lesions lead to increased muscle tone, a condition called hypertonia This results in stiffness and resistance to passive movement Reflexes Hyperactive reflexes are often present due to disrupted inhibitory signals from the brain Reflexes can be exaggerated or abnormal Spasticity Spasticity, characterized by sudden muscle contractions or spasms, is a common feature of UMN lesions Weakness or Paralysis Can occur due to disruption of signals between the brain and muscles Muscles may not receive appropriate signals for coordinated movement Examples of Conditions Stroke Traumatic brain injury Multiple sclerosis Cerebral palsy Certain spinal cord injuries can lead to UMN lesions Lower Motor Neuron Lesion (LMN): Location Occur outside the central nervous system, specifically withing the peripheral nervous system (PNS), which includes the nerves that extend from the spinal cord to the muscles Effect on Muscle Tone LMN lesions lead to decreased muscle tone, a condition called hypotonia This results in muscles feeling floppy and lacking resistance to passive movement Reflexes Reflexes are typically reduced or absent due to the interruption of signals between the spinal cord and muscles Atrophy Muscles may show signs of atrophy (wasting) due to the lack of neural input Weakness or Paralysis Severe muscle weakness or paralysis can occur due to the disruption of signals reaching the muscles directly Examples of Conditions Amyotrophic lateral sclerosis (ALS) Spinal muscular atrophy Peripheral nerve injuries Certain types of neuropathy can lead to LMN lesions Differences & Similarities The location of the lesion is the key distinguishing factor between UMN and LMN lesions UMN lesions involve damage within the CNS LMN lesions involve damage within the PNS Both types of lesions can lead to muscle weakness and impaired movement, but the patterns of weakness and other symptoms are different UMN lesions often result in increased muscle tone, hyperactive reflexes, and spasticity LMN lesions typically result in decreased muscle tone and reduced or absent reflexes The conditions that cause UMN and LMN lesions vary, with different underlying causes and mechanisms Neurological Signs & Symptoms: SPASTICITY vs RIGIDITY Spasticity Resistance of a limb to passive movement, abnormal increase of mm tone or stiffness of a muscle due to damage of UMN - Examples in Spinal cord injury, MS, Cerebral palsy, stroke, TBI, ALS ect. Generally only during mm stretch (not at rest) usually accompanied with increase tendon reflexes Velocity depending – meaning more noticeable with fast movements Difference in resistance from one direction to another Seen in pyramidal tract like corticospinal tract Rigidity Resistance throughout ROM due to over firing of UMN – examples in Parkinson's & Huntington's Mm tone is increased even at rest, present during PROM in all directions across individual joints Absence of synergy Seen in extrapyramidal lesions like rubiospinal or vestibulospinal tracts Cogwheel rigidity: hypertonic state w/ ratchet-like jerkiness Lead pipe rigidity: hypertonic state throughout ROM, simultaneous co-contraction of agonist & antagonist General Signs & Symptoms: Flaccidity: aka hypotonicity – decrease or loss of normal mm tone due to deterioration of LMN Weakness, contracture, postural imbalances Resting tremors, intention tremors (initiated with movement) Altered gait Circumduction gait in Hemiplegia or MS Bradykinesic or festinating gait seen in Parkinsons Decreased tissue health & edema leading to decubitus ulcers Seizures, speech dysfunction Bowel and bladder dysfunction Pain, behaviour and emotional changes Sensory and autonomic dysfunction Paresthesia or dysesthesia, increase as sweated or secretions, general abnormalities in temperature regulation Compensatory changes Mm hypertonicity, fascia restrictions, tendinitis, overuse syndromes Autonomic dysreflexia – SCI Definitions: Dysarthria Defective speech due to muscular dysfunction, mental function is intact Dyskinesia A defect in the ability to perform voluntary movement Dysmnesia Any impairment in memory Dysphagia Inability to swallow Dysphasia Impairment of speech resulting from brain lesion Dyspnea Laboured difficult breathing Dyspraxia A disturbance in control and execution of voluntary movements Dystonia Prolonged muscle contraction that causes twisting and repetitive movement or abnormal posture Dysesthesia Abnormal sensation on the skin Ataxia Defective muscular coordination Paresthesia Sensation of numbness, prickling, tingling Dysreflexia Individual with T6 or higher spinal cord injury experiences a life threatening uninhibited sympathetic response of the nervous system to a noxious stimulus Aphasia Inability to speak; may be due to lack of comprehension of words as opposed to dysphasia (inability to coordinate muscles of speech) Paralysis Temporary or permanent loss of function especially loss of sensation and voluntary control Can be spastic (upper motor neuron) Can be flaccid (lower motor neuron) Developmental Reflexes: What is a reflex? Involuntary, or automatic, action that the body does in response to a stimulus, without awareness Neonatal reflexes or primitive reflexes are the inborn behavioural patterns that develop during uterine life They should be fully present at birth and gradually inhibited by higher centres of the brain as the infant grows and develops 3 Types General body reflexes Moro / Startle reflex (integrated 2 – 4 months) Palmar / plantar grasp reflex (integrated 5 – 6 months) Walking / Stepping reflex (2 – 4 months) Asymmetric tonic neck reflex (6 months) Symmetric tonic neck reflex (9 – 11 months) Babinski's reflex (8 – 12 months) Facial reflexes Blind reflex (permanent) Auditory orienting reflex (permanent) Oral reflexes Rooting (3 – 4 months) Sucking Gag (permanent) Swallowing reflex Clinical Significance Developmental reflexes are automatic responses that are measured in terms of timing, strength, and symmetry and indicate how the signals are sent from the brain to the spinal cord and outward to individual muscles of the face, neck, torso, and extremities that are involved in postural control and movement Developmental reflex's are retained with some leaning disorders, ADHD, autism spectrum Startle/Moro reflex – leading to issues w/ balance and coordination Asymmetrical tonic neck reflex – leading to head control and balance issures Symmetrical tonic neck reflex – leading to poor posture and hand-eye coordination issues Palmar grasp reflex – leading to issues with fine motor skills Babinski reflex – leading to poor muscle tone, fatigue, vestibular related problems Rooting reflex – leading to issues with feeding