Upper and Lower Motoneurons for the Head Objectives

Upper and Lower Motoneurons for the Head Objectives Know the locations of cranial nerve motor nuclei Describe the effects of motor cranial nerve lesions Describe how the corticobulbar tract innervates cranial nerve motor nuclei and its significance in lesions Describe how corticobulbar lesions affect the functions of CN V, VII, and XII

Functional Distinctions FUNCTION COMPONENT DEFICITS Start Basal Ganglia Spontaneous Movements Move Cerebral Cortex Brainstem, Spinal cord Roots/peripheral nerves Plan Cerebellum Ataxia Adjust Cerebellum Ataxia Weak/Paralyzed Balance/EyeMove Cerebellum Loss of balance Nystagmus Chris Cohan, Ph.D. Dept. of Pathology/Anat Sci University at Buffalo

Symptoms of Lesions LMN Lesions 1. Paresis Flaccid, ipsilateral to injury 2. Decreased tendon reflexes 3. Decreased muscle tone 4. Severe muscle atrophy 5. Fasciculations UMN Lesions 1. Paresis/paralysis 2. Increased muscle tone- Spasticity 3. Increased tendon reflexes 4. Babinski sign

How do these symptoms apply to muscles of the head? LMN Lesions 1. Paresis/paralysis - Flaccid, ipsilateral 2. Decreased tendon reflexes 3. Decreased muscle tone 4. Severe muscle atrophy (wasting) 5. Fasciculations UMN Lesions 1. Paresis/paralysis - Spasticity 2. Increased tendon reflexes 3. Increased muscle tone 4. Babinski sign Involving spinal motoneurons (or cranial nerve motor nuclei) Involving corticospinal and cortico-bulbo-spinal tracts The head has midline structures that are attached to muscles on both sides of the head. If muscles on one side are weak, the position of the structure will be shifted off the midline. jaw uvula head (via sternocleidomastoid) tongue

Head Movements CN III, IV, VI CN V CN IX, X CN XII CN VII CN XI

Motor Cranial Nerves Controlled by 2 component system also UMN- corticobulbar fibers LMN- motor cranial nerves Thalamus Cerebral Cortex Basal Ganglia Cranial nerves head muscles Cerebellum Brainstem Corticobulbar T Body muscles Spinal Cord

Brainstem LMNs Cranial Nerve Motoneurons: midbrain medulla CN III, IV, VI extrinsic eye muscles CN V jaw muscles CN VII facial muscles CN IX, X = Nucleus Ambiguus for larynx, pharynx CN XII tongue midbrain pons medulla CN XI trapezius, sternocleidomastoid

Motor Cranial Nerves III IV V VI VII IX, X XII XI

Symptoms of LMN Lesions Paresis Flaccid, ipsilateral to injury Decreased tendon reflexes Decreased muscle tone Severe muscle atrophy Fasciculations not observable for CNs midbrain pons V VII medulla ambiguus What effect does a cranial nerve lesion have on head structures? Weakness on one side XII XI

Motor Cranial Nerve Lesions Cranial Nerve Lesions ipsilateral effects on muscles CN III, IV, VI CN V CN VII Nuc Ambiguus CN XII eye moves toward strong side jaw* deviates to weak side paralysis of facial muscles loss of gag reflex/swallowing, hoarseness, uvula* deviates to strong side, palate droop tongue* deviates to weak side See CN review chart in handout CN XI *Midline structures deviate to one side when muscles are weak/paralyzed on one side. weakness in shoulder shrug, head turn to opposite side trapezius sternocleidomastoid

Motor Cranial Nerve Lesions Cranial Nerve Lesions ipsilateral effects on muscles CN V jaw deviates to weak side Nuc Ambiguus uvula deviates to strong side CN XII tongue deviates to weak side Muscle Midline pulls structures away from deviate midline to one deviation side when to strong muscles side are weak/paralyzed on one side. Muscle pulls toward midline deviation to weak side Moves toward strong side Moves toward weak side weak Lateral pterygoids pull jaw towards center Uvula pulled away from midline Tongue pulled towards midline

Motor Cranial Nerve Lesions tongue deviates toward side of lesion

CN VII Bells Palsy Paralyzed side less wrinkling can t close eye decreased nasolabial fold drooping corner of mouth Bell s

Facial weakness can be assessed by asking the patient to raise eye brows Weak side close eyes (not shown here) smile Weak side forehead eye lid nasolabial fold mouth

Motor cranial nerves (LMNs) are controlled by Upper Motoneurons for the head

Control of Cranial Nerve Motoneurons For UMN supply: (III, IV, VI) discussed previously (frontal eye field) V VII Nuc. Ambiguus (IX, X) XII XI Know these V VII XII Nuc ambiguus midbrain pons medulla XI

Corticobulbar Fibers UMN CST Arise in face area of precentral gyrus travel with CST to brainstem pass in genu of internal capsule Corticobulbar fibers synapse on cranial nerve motor nuclei bilaterally or unilaterally. Corticobulbar lesions on 1 side have little effect Corticobulbar lesions on 1 side cause deficits V VII XII Nuc ambiguus travel together

Corticobulbar Innervation Bilateral Innervation: CN V CN VII upper face muscles Corticobulbar lesions have little effect Unilateral (Contralateral) Innervation: CN VII - lower facial muscles CN XII tongue Corticobulbar lesions cause deficit

LMNs to face 1. UMN Control of CN VII 2 groups: upper/lower face LMN to upper face supplied bilaterally by corticobulbars LMN to lower face supplied only by contralateral corticobulbars Facial Motor Nucleus CN VII corticospinal and corticobulbar fibers To upper face To lower face

LMNs to face 1. UMN Control of CN VII 2 groups: upper/lower face LMN to upper face supplied bilaterally by corticobulbars LMN to lower face supplied only by contralateral corticobulbars Facial Motor Nucleus CN VII corticospinal and corticobulbar fibers To upper face To lower face

LMNs to face 1. UMN Control of CN VII 2 groups: upper/lower face LMN to upper face supplied bilaterally by corticobulbars LMN to lower face supplied only by contralateral corticobulbars Facial Motor Nucleus CN VII corticospinal and corticobulbar fibers To upper face To lower face

1. UMN Control of CN VII Lesions of corticobulbars on one side cause weakness or paralysis of the lower face on the opposite side: decreased nasolabial fold drooping mouth Lower face droop on side opposite lesion (usually + corticospinal deficit)

2. UMN Control of CN XII Corticobulbar supply to CN XII is mostly contralateral. Corticobulbar lesions produce transient contralateral weakness in tongue muscles. R L Tongue deviates to opposite/weak side (usually + corticospinal deficit) XII

Case Study A 60-year old hypertensive man awoke one morning to find he could not move his right arm. His wife noticed that the right side of his mouth drooped, he was drooling, and when she spoke to him his answers were slow and he only said a few words, Me sick.

Explanation of Neurological Findings 1. Paralysis of right arm 2. Increased muscle tone on right arm 3. Increased DTRs on right arm 5. Rt mouth drooped, drooling; Could wrinkle forehead/close both eyes; Smiling: only left side of mouth moved 6. Language comprehension: good Speech: slow; uses few words UMN lesion CN VII-related Aphasia- Broca s Localization = cortex

Explanation of Neurological Findings R L VII

Lesion Localized This area is within the territory of branches of the middle cerebral artery, which limits the lesion and its deficits to this particular location.