OS 202 Approach to Weakness PDF

OS 202: HUMAN BODY AND MIND 1: INTEGRATION AND CONTROL SYSTEMS SYSTEMATIC APPROACH TO MOTOR COMPLAINTS UPCM 2029 | Dr. Godfrey T. Robeniol | LU3 A.Y. 2024-2025 OUTLINE I.​ Motor Neuron System III.​ Final...

OS 202: HUMAN BODY AND MIND 1: INTEGRATION AND CONTROL SYSTEMS SYSTEMATIC APPROACH TO MOTOR COMPLAINTS UPCM 2029 | Dr. Godfrey T. Robeniol | LU3 A.Y. 2024-2025 OUTLINE I.​ Motor Neuron System III.​ Final Common Pathway A.​ Motor System Overview A.​ Motor Unit II.​ Direct Activation B.​ Neuromuscular Pathways Transmission A.​ Pathway IV.​ Reflex B.​ Blood Supply of the V.​ Cerebellar System Motor Cortex VI.​ Localization of Lesions C.​ Upper and Lower Causing Paralysis or Motor Neurons Weakness D.​ Motor Areas of the A.​ Localization of Cerebral Cortex Lesions E.​ Corticobulbar Tract B.​ Summary F.​ Corticospinal Tract VII.​ Appendix Figure 3. To move our facial muscles, we need 2 neuronal systems working together: G.​ Somatic The Upper Motor Neuron originates in the cerebral cortex and the Lower Motor Representation of the Neuron originates in the brainstem. The second is more appropriately referred to Corticospinal and as the Cranial Nerve Motor Nuclei Corticobulbar Tracts ​ The motor system is responsible for the planning, coordination, and execution of movement. LEARNING OBJECTIVES ○​ Ataxia is defined as uncoordinated movements. 1.​ Trace the corticospinal pathway from the precentral gyri through ​ Conditions that injure the Upper or Lower Motor Systems are called the projection fibers in the subcortical white matter into the muscle paralysis or weakness. brainstem & spinal cord. PARALYSIS 2.​Differentiate weakness due to lesions in the corticospinal tract, ​ Loss of voluntary movement due to interruption of one of the motor peripheral nerve, or neuromuscular junction pathways at any point from the cerebrum to the muscle fiber. 3.​Localize lesions that cause weakness ​ Plegia: severe paralysis (0-1 out of 5 muscle strength) ​ Hemiplegia: severe paralysis of one side of the body I.​ MOTOR NEURON SYSTEM ​ Quadriplegia: severe paralysis of all four extremities ​ To move parts of our body (e.g. arm), 2 neuronal systems are ​ Paraplegia: severe paralysis of the legs needed to work together: ​ Paresis: lesser degree of paralysis (2-4 out of 5 muscle strength) ○​ Upper Motor Neuron (Red) ○​ Hemiparesis: weakness of one side of the body ​ Originates in the the cerebral cortex ​ Synapses with the lower motor neuron WEAKNESS ○​ Lower Motor Neuron (Yellow) ​ Weakness can have a lot of meaning depending on the context or ​ Arms and Legs: Originates in the Ventral/Anterior Horn of the patient’s history Spinal Cord [Refer to Figures 1 and 2] ○​ Weakness can be referred to as: ​ Facial Muscles: Brainstem (Cranial Nerve Motor Nuclei) [Refer ​ Body Malaise to Figure 3] ​ Lack of motivation ​ Depression, ​ Incoordination of Movement ​ Rigidity ○​ The History and Physical Examination should help determine what the patient actually means ○​ Real muscle weakness is due to the inability of a muscle to contract with normal strength because of an injury/lesion in the motor fibers of the: ​ Cerebral cortex ​ Brainstem ​ Spinal cord ​ Peripheral nerves ​ Neuromuscular junction ​ Muscle A.​ MOTOR SYSTEM OVERVIEW Figure 1. To move our arm, we need 2 neuronal systems: The Upper Motor Neuron originates in the cerebral cortex, while the Lower Motor Neuron originates in the anterior horn of the spinal cord. Figure 4. Overview of pathways ​ In order for a person to move normally, one must need: Figure 2. To move our leg, we also needs 2 neuronal systems: The Upper Motor ○​ Muscle Strength Neuron originates in the cerebral cortex, while the Lower Motor Neuron originates ○​ Coordination in the anterior horn of the spinal cord ○​ Must not be spastic or rigid ​ All of the structures described in the diagram allow for you to move your body and control your muscle movement PRIMARY MOTOR CORTEX ​ Location: Precentral gyrus in the frontal lobe (Brodman area 4). ​ Large areas allocated for face, tongue, and hand movements due to specialized functions. ○​ Major source of upper motor neurons ​ Upper motor neurons (UMNs) for: ○​ Face and hands: Lateral parts of the primary motor cortex. ○​ Trunk: Superior part. ○​ Legs: Medial part. Trans #3 TG29: Tiam-Lee, Timbulan, Tolentino, P., Tolentino, V., Uy, F., Uy, M., Valimento TH: Magsuay 1 of 9  OTHER MOTOR AREAS OF THE CEREBRAL CORTEX ​ Tracts: ○​ Reticulospinal ​ Regions of electrically excitable cortex where isolated ○​ Vestibulospinal movements can be evoked with minimal stimuli: ○​ Rubrospinal ○​ Primary Motor Cortex (Area 4) ○​ Tectospinal ○​ Premotor Area: ​ Coordination of movement comes from: ○​ Lateral Premotor Cortex (Area 6a) ○​ Thalamus ○​ Supplementary Motor Area: ○​ Cerebellum ○​ Medial Premotor Cortex (Area 6b) ○​ Basal ganglia ○​ Primary Somatosensory Cortex (Areas 3, 1, 2) ○​ Superior Parietal Lobule (Areas 5, 7) NEUROTRANSMITTERS ○​ Anterior Cingulate Motor Area ​ Upper to Lower Motor Neuron Synapse ○​ Frontal Eye Fields (Area 8) ○​ Neurotransmitter: Glutamate. ○​ Broca's Area (Area 44) ○​ Location: Synapse occurs in: ​ Cranial nerve motor nuclei (Corticobulbar Tracts). ​ Anterior horn of the spinal cord (Corticospinal Tracts). ​ Neuromuscular Junction (NMJ) ○​ Neurotransmitter: Acetylcholine. ○​ Links lower motor neurons to muscle fibers. B.​ VASCULAR SUPPLY OF MOTOR SYSTEM ​ Middle Cerebral Artery (MCA) ○​ Supplies areas controlling face, arm, and hand. ○​ Occlusion: ​ Contralateral weakness affects face and arm more than leg. ​ Arm weakness > leg weakness. ​ Anterior Cerebral Artery (ACA) ○​ Supplies areas controlling the leg. Figure 5. Brodmann areas of the brain ○​ Occlusion: ​ Contralateral weakness affects leg more than arm. ​ Leg weakness > arm weakness. DIRECT ACTIVATION PATHWAYS/DESCENDING TRACTS ​ Called “direct pathways” because these tracts descend uninterruptedly from the cerebral motor cortex to the spinal cord and brainstem ​ Function: To initiate & control skilled voluntary activity, under conscious control ​ Glutamate is the neurotransmitter ​ General Pathway: ○​ Primary Motor Cortex → Corona Radiata → Posterior Limb of Internal Capsule. ○​ At brainstem: Fibers diverge into corticospinal and corticobulbar tracts. Figure 7. Arterial Blood Supply of the Motor Cortex (MCA; ACA) C.​ KEY ANATOMIC RELATIONSHIPS ​ Internal Capsule ○​ Posterior Limb: Contains corticospinal and corticobulbar fibers. ​ Lesions cause dense contralateral weakness: ​ Severity is equal in arm and leg. ​ Cerebral Peduncle ○​ Location: Middle 2/3 in the midbrain. ○​ Corticospinal tracts continue here, while corticobulbar fibers terminate. ​ Spinal Cord ○​ Lateral Corticospinal Tracts ​ Arm fibers: Medial. Figure 6. Simplified diagram of descending pathways ​ Leg fibers: Lateral. ​Clinical Implication: Corticobulbar Tract ○​ Tumor from outside spinal cord → Ipsilateral leg weakness. ​ Originate in the motor cortex and terminate in cranial motor nerve ○​ Tumor from inside spinal cord → Ipsilateral arm weakness. nuclei within the brainstem. ○​ Anterior Horn Cells ○​ Brainstem was used to be called “bulb” ​ Synapse point for corticospinal tracts with lower motor ​ Synapse with cranial motor nerve nuclei in: neurons. ○​ Midbrain, Pons, or Medulla. ​ Control cranial nerves with motor functions: ○​ CN III (Oculomotor), CN IV (Trochlear), CN VI (Abducens), CN V (Trigeminal), CN VII (Facial), CN IX (Glossopharyngeal), CN X (Vagus), CN XI (Spinal Accessory), CN XII (Hypoglossal). Corticospinal Tract ​ Begins in the cerebral cortex and ends in the spinal cord ○​ Also referred to as the Pyramidal Tract ​ Fibers continue to spinal cord: ○​ 90% Decussate at medullary pyramids → Lateral funiculus (Lateral Corticospinal Tracts). ○​ 10% Do Not Decussate → Anterior funiculus (Anterior/Ventral Corticospinal Tracts). ​ In order to move effectively, the Extrapyramidal system is needed as well ○​ Basal Ganglia ○​ Cerebellum ○​ Thalamus ○​ Vestibulospinal tract ○​ Rubrospinal tract ○​ Tectospinal tract ○​ Reticulospinal tract CONTROL CIRCUITS ​ Cerebellum & basal ganglia ​ Works with cerebral cortex for fine-tuning of movements INDIRECT ACTIVATION PATHWAYS OS 202 Approach to Weakness 2 of 9  UPPER MOTOR NEURONS ​ Motor neurons that project from the primary motor cortex ​ Includes cortical motor neurons and their projections to the: ○​ Spinal cord, directly (corticospinal tract) or via the brainstem motor pathways (indirect pathways) ○​ Brainstem motor nuclei (corticobulbar tract) Table 1. PATHWAYS OF THE UPPER MOTOR NEURON SYSTEM DIRECT PATHWAYS INDIRECT PATHWAYS** Corticospinal tract* Corticorubrospinal tract* Corticobulbar tract Corticoreticulospinal tract* Corticovestibulospinal tract* Corticotectospinal tract* Figure 8. Somatotropic representation of the corticospinal and corticobulbar tracts * These tracts are pathways through which the cortex influences the spinal motor neurons II.​ DIRECT ACTIVATION PATHWAYS ** The indirect pathways will be discussed further in LU4 LOWER MOTOR NEURONS ​ Motor neurons that synapse with the upper motor neurons and project out of the CNS to reach the muscle cells in the periphery ​ Includes the alpha motor neurons in the: ○​ Spinal cord - anterior horn cells & peripheral motor nerves (corticospinal tract) ○​ Brainstem - brainstem motor nuclei & cranial motor nerves (corticobulbar tract) SUMMARY ​ The following table describes the upper and lower motor neurons of the corticospinal and corticobulbar tracts Table 2. UMNs and LMNs OF THE DIRECT PATHWAYS NEURONS CORTICOSPINAL TRACT CORTICOBULBAR TRACT Upper Motor Motor neurons in the Neurons cerebral cortex & their axons Anterior horn cells in the Cranial nerve motor nuclei Lower Motor spinal cord & their in the brainstem & their Neurons peripheral nerves cranial nerves Figure 9. Corticospinal and corticobulbar tracts A.​ DESCENDING PATHWAYS CORTICOBULBAR TRACT ​ Pathway: 1.​ Primary Motor Cortex → Corona Radiata → Posterior Limb of Internal Capsule. 2.​ Cerebral Peduncle → Pons. 3.​ Synapses with cranial motor nerve nucleus in the pons. 4.​ Peripheral nerve (cranial nerve) innervates facial/bulbar muscles. CORTICOSPINAL TRACT Pathway of Upper Extremities ​ Pathway: 1.​ Primary Motor Cortex → Corona Radiata → Posterior Limb of Figure 11. Diagram showing the upper motor neuron (UMN, red) Internal Capsule. and lower motor neuron (LMN, yellow) in the corticospinal tract. 2.​ Cerebral Peduncle → Pons → Medulla. 3.​ Decussates at medullary pyramids → Lateral funiculus of UPPER VS LOWER MOTOR NEURON PARALYSIS cervical spinal cord. 4.​ Synapses with lower motor neurons in the anterior horn of the cervical spinal cord. 5.​ Peripheral nerve innervates the skeletal muscles of the arm. Pathway of Lower Extremities ​ Pathway: 1.​ Primary Motor Cortex → Corona Radiata → Posterior Limb of Internal Capsule. 2.​ Cerebral Peduncle → Pons → Medulla. 3.​ Decussates at medullary pyramids → Lateral funiculus of: a.​ Cervical, Thoracic, Lumbar spinal cord. 4.​ Synapses with lower motor neurons in the anterior horn of the lumbar spinal cord. 5.​ Peripheral nerve innervates skeletal muscles of the leg. Figure 12. Upper (red) and Lower (yellow) Motor Neurons. ​ The red neuron whose cell body is in the motor cortex down to its axon is the UMN ​ The yellow neuron whose cell body is in the anterior horn of the spinal down down to its peripheral nerve is the LMN Table 3. UPPER AND LOWER MOTOR NEURON PARALYSIS LOWER MOTOR NEURON UPPER MOTOR NEURON (NUCLEAR-INFRANUCLEAR) (SUPRANUCLEAR) PARALYSIS PARALYSIS Caused by an upper motor Caused by a lower motor neuron neuron lesion lesion Figure 10. The corticospinal (red and blue) and corticobulbar tracts (yellow). Muscles are affected in groups, Individual muscles may be never individual muscles B.​ UPPER AND LOWER MOTOR NEURONS affected OS 202 Approach to Weakness 3 of 9  Pronounced atrophy, up to 70% Slight atrophy due to disuse of total bulk (Denervation (Disuse atrophy) atrophy) Flaccidity and hypotonia of the affected muscles with loss of Spasticity with hyperactivity of tendon reflexes the tendon reflexes and extensor plantar response (Babinski sign) Plantar reflex, if present is of normal flexor type No fasciculations Fasciculations may be present Abnormal EMG, with fibrillations, fasciculations, positive sharp Normal electromyography & waves nerve conduction velocity (EMG-NCV) Abnormal NCV, with denervation potentials ​ Spastic Paralysis ○​ An upper motor neuron type of paralysis caused by a lesion anywhere in the course of UMN Figure 14. Lesions in the corticobulbar tract which leads to (L) central facial palsy [UMN] and (R) peripheral facial palsy [LMN] ○​ Muscles become spastic of stiff ○​ If the UMN is damaged, the LMN can still lead to some movement of the muscle, but the abnormal signs mentioned in the table will be observed ​ Flaccid Paralysis ○​ A lower motor neuron type of paralysis caused by a lesion anywhere in the course of the LMN ○​ Cells become flaccid ○​ If the LMN is damaged, paralysis will be more severe because denervation occurs where there is no more neuron sending impulses to the muscle ​ UMN controls the activity of the LMN ○​ Analogy: Like a teacher controlling a student. If the teacher (UMN) gets sick, the student (LMN) may still learn and function but may be misguided (may be stressed and hyperactive). If the student (LMN) becomes sick, there will be learning at all, hence, worse. Figure 15. Illustration of the difference between central and peripheral palsy. C.​ CORTICOBULBAR TRACT AND FACIAL NERVE ​ For central palsy, the lesion is in the left motor cortex (contralateral to the side of paralysis) Refer to Figure 13. For peripheral palsy, the lesion is in the right facial nerve or right ​ Multiple corticobulbar fiber tracts (UMNs) synapse with the facial facial motor nuclei in the pons (ipsilateral to the side of the paralysis). cranial nerve motor nuclei (LMNs) in the pons ○​ Some fiber tracts decussate (red and yellow) III.​ FINAL COMMON PATHWAY ○​ Some fibers do NOT decussate (green) ​ Essentially the lower motor neuron: ​ From the facial cranial nerve motor nuclei in the pons, nerves ○​ From neuronal body in brainstem to motor cranial nerve project towards the face to innervate the upper and lower halves ○​ From neuronal body in spinal cord to peripheral nerve ○​ Lower half of the face is innervated ONLY by contralateral ​ This final common pathway is influenced and controlled by cerebral motor cortex (yellow) multiple neuronal systems (i.e. UMN system) ○​ Upper half of face has bilateral innervation (contralateral - red; ○​ Thalamus ipsilateral - green) ○​ Cerebellum ○​ Motor cortex ​ Controls the lower motor neurons via the corticospinal and corticobulbar tracts ○​ Basal ganglia ○​ Superior colliculus, vestibular nuclei, reticular formation, red nucleus ​ It includes the axons or the nerves that the lower motor neurons send out to innervate the muscles[2028 Trans] ​ Motor unit = lower motor neuron + muscle it innervates Figure 13. The corticobulbar tract and facial nerve FACIAL PALSY ​ Central Facial Palsy ○​ Caused by supranuclear lesions (UMN lesion) in the cerebral cortex or corticobulbar tract ​ E.g., due to stroke or hemorrhage in the frontal lobe ○​ Paralysis of the lower half of the face contralateral to the lesion ​ Upper half of the right side of the face will not be weak since it Figure 16. The final common pathway influenced and controlled by many neuronal systems. is innervated by both cerebral hemispheres. ​ Peripheral Facial Palsy ○​ Caused by lesions (LMN lesion) in the facial nerve nucleus or lesion of the facial nerve ○​ Paralysis of the entire half of the face ipsilateral to the lesion (e.g., Bell’s palsy) OS 202 Approach to Weakness 4 of 9  Figure 19. Transmission of action potential from the nerve to the muscle along the neuromuscular junction ​ Action potential reaches the distal end of an axon ○​ Acetylcholine (ACh) is released into the neuromuscular junction ​ Acetylcholine is the only neurotransmitter used in the final common pathway ○​ Acetylcholine attaches to the acetylcholine receptors in the muscle. Figure 17. The course of the final common pathway (essentially the LMN) as it goes ​ This generates an excitatory postsynaptic potential (endplate out to the muscles it will innervate. potential) that propagates in the muscle that leads to muscle A.​ MOTOR UNIT contractions ​ Includes the lower motor neuron plus all the muscle fibers it ​ Diseases in the neuromuscular junction that cause destruction and synapses with/it innervates. reduction in the number of acetylcholine receptors (e.g., Myasthenia gravis) manifest as fluctuating or fatigable muscle weakness. ○​ This weakness is aggravated by repeated movements and the weakness improves with rest. IV.​ REFLEX ​ Most elementary form of motor coordination ○​ E.g. Stretch reflex ​ Stereotyped response to a specific sensory stimulus ​ Most common example is the kicking forward of the leg upon tapping the patella From Trans 2028 ​ Reflex is composed of afferent and efferent arcs REFLEX ARC Figure 18. The LMN innervating muscle fibers. ​ Recall: injury to the lower motor neuron causes a flaccid paralysis Reflex Arc of the Patellar Reflex and may also be accompanied by fasciculations and fibrillations. ○​ Lower motor neuron can be very irritable and may send abnormal impulses FASCICULATIONS ​ Sporadic contraction (involuntary contractions) of muscle fibers in one or more several motor units. ○​ Visible: one can feel and see muscle fasciculations. ○​ EMG: large, spontaneous muscle action potential. ​ This is caused by the injury to the lower motor neuron which causes excitatory abnormal discharges coming from the neuronal body or its axon. ​ There are normal/benign fasciculations ○​ Fasciculations presented by the upper or lower eyelid due to excess fatigue ○​ Muscle fasciculations after drinking coffee. FIBRILLATIONS ​ Isolated contraction of a single muscle fiber. ○​ Cannot be seen by a naked eye; may be felt but not seen ○​ EMG: small, repetitive, short duration potential Figure 20. Patellar Reflex Arc ​ May happen if the abnormal excitatory discharges come from the ​ The process of the reflex arc of the patellar reflex is as follows: more distal nerve fibers innervating a single muscle fiber ○​ (1) Upon tapping the patellar tendon of the quadriceps muscle on ​ Caused by death of LMN[2028 Trans] the knee, the quadriceps muscle and the muscle spindle are stretched ○​ (2) The stretch stimulus is then transmitted via the afferent nerve B.​ NEUROMUSCULAR TRANSMISSION to the dorsal root ganglion and to the dorsal horn of the spinal cord ○​ (3) The afferent nerve stimulates the anterior horn cell (lower motor neuron) ○​ (4) The excitatory impulse from the anterior horn cell travels via the efferent nerve to cause contraction of the quadriceps muscle ​ The stretch reflex is monosynaptic ○​ There is only one synapse between neurons. This synapse is in the anterior horn of the spinal cord. ​ The stretch reflex is controlled by higher centers in the nervous system, although this reflex occurs at the spinal cord level only and functions without the need of the higher centers. ​ A lesion in the afferent nerve or efferent nerve (the LMN) causes hyporeflexia or areflexia (decreased or no reflex response). ​ A lesion in the upper motor neuron causes hyperreflexia. V.​ CEREBELLAR SYSTEM CEREBELLAR INFLUENCE ON CORTICOSPINAL TRACT Corticospinal Tract OS 202 Approach to Weakness 5 of 9  Figure 24. Cerebellar Lesion Figure 21. Corticospinal Tract ​ Cerebellar lesions cause ataxia or incoordination of movement ​ Figure 21 shows the corticospinal tract as it goes down to synapse since the cerebellum coordinates movement with the anterior horn cell in the spinal cord ​ Unlike corticospinal tract lesions, cerebellar lesions DO NOT cause ​ The axon of the anterior horn cell (peripheral nerve) innervates a muscle weakness muscle ​ Because of the 2 decussations, a cerebellar lesion causes ataxia ipsilateral to the lesion. VI.​ LOCALIZATION OF LESIONS CAUSING PARALYSIS OR WEAKNESS TYPES OF PARALYSIS ​ Spastic Paralysis: Due to UMN lesions ​ Flaccid Paralysis: Due to LMN lesions ○​ Abnormal signs observed in spastic and flaccid paralysis were previously discussed in Table. ​ Fluctuating Weakness: Due to neuromuscular junction disorders A.​ LOCALIZATION OF LESIONS Figure 22. Corticospinal Tract Lesion ​ Corticospinal tract lesions cause muscle weakness (paralysis) ​ A lesion in the motor cortex causes paralysis of the extremities contralateral to the lesion Cerebellum’s Influence Figure 25. Corticospinal and corticobulbar tracts Table 4. LESION LOCATIONS AND CORRESPONDING CONSEQUENCES (assume affected region is contralateral to lesion unless stated otherwise) See Appendix for figures of respective lesion locations LOCATION OF LESION CONSEQUENCE Brain Face: Unaffected Small lacunar Infarct Arm: Spastic Paralysis Leg: Unaffected Face: Central Weakness Arm: Spastic Paralysis Middle Cerebral Artery (MCA) Infarct Leg: Spastic Paralysis (Mild) Figure 23. Dento-thalamo-cortical & Dentato-rubro-thalamo-cortical tracts (green) Clinical correlation: Differential weakness ​ Dentato-thalamo-cortical tract & of arm and leg dentato-rubro-thalamo-cortical tract Face: Unaffected ○​ The tracts in green from the dentate nuclei in the cerebellum ending in the contralateral motor cortex Arm: Spastic Paralysis (Mild) ○​ Throughout the entire course of these tracts, there are 2 Anterior Cerebral Artery (ACA) Infarct Leg: Spastic Paralysis decussations: ​ (1) In the dentato-thalamic fibers Clinical correlation: Differential weakness ​ (2) In the corticospinal tract as it crosses to the other side at of arm and leg the level of the medullary pyramids Face: Central Weakness ○​ Since there are 2 decussations, the cerebellum controls the muscles on the ipsilateral side Arm: Spastic Paralysis Internal Capsule Leg: Spastic Paralysis Clinical correlation: Dense hemiplegia of arm and leg (same degree of weakness) Face: Ipsilateral peripheral weakness Arm: Spastic Paralysis Brainstem Leg: Spastic Paralysis OS 202 Approach to Weakness 6 of 9  Clinical correlation: Crossed signs (peripheral facial weakness on one side with contralateral UMN weakness) Face: Ipsilateral peripheral weakness Arm: Unaffected Facial nerve Leg: Unaffected Clinical correlation: Bell’s Palsy Spinal Cord Face: Unaffected Upper Cervical Spinal Cord (above C5; one Arm: Ipsilateral Spastic Paralysis side only) Leg: Ipsilateral Spastic Paralysis Face: Unaffected Arm: Bilateral Spastic Paralysis Entire Upper Cervical Cord (Transverse Leg: Bilateral Spastic Paralysis Myelopathy) Clinical correlation: Quadriplegia or quadriparesis (paralysis of both arms and legs) Face: Unaffected Cervical Spinal Cord Arm: Ipsilateral Flaccid Paralysis (C5-C8; one side only) Leg: Ipsilateral Spastic Paralysis Face: Unaffected Cervical Roots or Arm: Ipsilateral Flaccid Paralysis Brachial Plexus Leg: Unaffected Face: Unaffected Thoracic Spinal Cord Arm: Unaffected (one side only) Leg: Ipsilateral Spastic Paralysis Face: Unaffected Entire Thoracic Spinal Arm: Unaffected Cord (Transverse Leg: Bilateral Spastic Paralysis Myelopathy) Clinical correlation: Paraplegia or paraparesis (paralysis of both legs) Face: Unaffected Lumbar Spinal Cord Arm: Unaffected (one side only) Leg: Ipsilateral Flaccid Paralysis Face: Unaffected Arm: Unaffected Lumbar Roots or Leg: Ipsilateral Flaccid Paralysis Plexus Clinical correlation: No loss of bladder or bowel control as seen in lumbar spinal cord lesions B.​ SUMMARY Figure X. Distinguishing Muscle Weakness based on Localization ​ Neuropathies usually cause more prominent distal muscle weakness. ​ Myopathies cause more proximal muscle weakness. ​ Neuromuscular junction disorders (e.g. myasthenia gravis) typically present with fluctuating weakness. ○​ Normal function returns after rest. OS 202 Approach to Weakness 7 of 9  APPENDIX Figure 26, 27, 28. Lesion Locations within the Brain and Corresponding Paralysis and Weakness OS 202 Approach to Weakness 8 of 9  Figure 29, 30, 31. Lesion Locations within the Spinal Cord and Corresponding Paralysis and Weakness OS 202 Approach to Weakness 9 of 9