Cavernous Sinus Thrombosis

Neuro tutoring Block 7 Week 4 1. Define the following: -MLF: • Yokes eyes together so that your gaze is conjugated together in all directions • Controls contralateral CN III nucleus from CN VI nucleus • Relays VOR -PPRF: • Conveys input from cortex to CN VI nucleus -Abducens nucleus: • Horizontal gaze center 2. What are the functions and components of saccades? • Really fast eye movements 700 degrees/sec • Rapid eye movements to bring target of interest into the field of view • Vision is transiently suppressed during saccadic movements • Voluntary or reflex • Scanning scenes, pictures, reading • Pathway initiated by frontal eye field: precentral/middle frontal gyri • 2 Pathways: o Precentral/middle frontal gyri superior colliculi PPRF saccades via CN VI o Precentral/middle frontal gyri PPRF saccades via CN VI 3. What are the functions and components of smooth pursuit? • Reflex (not voluntary) • Allows for stable viewing of moving objects • Used with VOR suppression (cerebellum and vestibular nuclei) • Cortical damage causes deficit of smooth pursuit to ipsilateral side • Extrastriate cortex/frontal eye field pontine nuclei floculus vestibular nuclei (juxtavestiform body) CN VI MLF CN III 4. What are the functions and components of vergence? • Eye movements maintain gaze fixation as the target moves towards and away from viewer • Convergence: medial rectus • Divergence: lateral rectus • Pretectal pathway (not via MLF) o Why you can look up with Parinauds 5. What deficit would you see with 1 ½ syndrome? Where is the lesion? • MLF and PPRF lesion (left for this example) • Can’t look to the left (ipsilateral gaze palsy)

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Nystagmus with right eye (contralateral INObeckoning to other eye to follow)

6. Describe the lesion and deficits associated with Parinauds Syndrome: • Compression of the dorsal midbrain and pretectal area • Causes: pineal tumor, hydrocephalus • Impaired vertical gaze • Impaired papillary constriction/dilation o But you can accommodate • Loss of upward gaze • Ptosis • Convergence/retraction nystagmus 7. What is Internuclear opthalamoplegia and where is the lesion? (INO) • Classic MLF lesion • Impaired eye adduction (ipsilateral) • Eye can adduct during convergence (pathway is pretectal) • MS, ALS, pontine infarct, MLF neoplasm 8. What is the UMN pattern of weakness? • Upper limb o Extensors more affected (flexors are stronger) o Arm flexed at elbow • Lower limb o Stronger extensors o leg tonically extended at knee, ankle • Antigravity muscles less affected by UMN lesion o person with this lesion can still walk, stand, carry • Babinski sign: dorsiflexion is abnormal 9. Where is the deficit with diabetic peripheral neuropathy? • Afferent from patellar tendon(lesion seen here) DRG interneuron  efferent  quads (knee extension) o Lesion is before you get sensory info. into the spinal cord 10. Where are the various locations for LMN lesions? • Anterior horn cell (this is where lower motor neuron begins) o Lesion: neuronopathy o Muscle flaccidity (losing excitation into the muscle o Atrophy o Examples:  ALS, polio • Spinal Root

o Lesion: radiculopathy o Very painful o Weakness, atrophy • • •

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Plexus (ie. brachial plexus or lumbosacral) o Pancoasts tumor o See larger, more regional deficits (ie. your entire arm has weakness) Peripheral nerve Lesion o Ie. Carpal Tunnel NMJ o Myastenia Gravis (MG): Ach receptor antibodies o Lambert-eaton MG: caused by different antibody not to the receptor, decreases Ca2+ influx o Botulism: inhibits docking via cleavage of V/T snares Muscle o Ie. Muscular Dystrophy o Localize with EMG

11. Where are the various locations for UMN lesions? • Can see hyperreflexia, but can take up to 6 weeks to occur o You would see an initial flaccidity if someone just came into emergency room • Blood supply lesions: o MCA infarct: face, hands, arm, trunk weakness o ACA: legs and feet o **ACA-MCA Watershed: arm weakness > leg weakness; man-in-barrel syndrome o **MCA-PCA Watershed: face weakness 12. Cranial Nerves: functions and lesions CN I • Olfactory • Causes: trauma, lesion, miangioma • Olfactory bulb tract entorhinal cortex (inferior medial temporal lobe) CNIII • Nucleus is at the midbrain • Innervates a bunch of eye muscles: superior rectus, inferior rectus, medial rectus, inferior oblique, levator palpebrae, sphincter papillae • Dysfunction: o “Down and Out” o Ptosis: levator palpebrae o Lateral strabismus (unopposed abduction) o Vertical diplopia o Papillary dilation (blown pupil) • **Posterior communicating aneurysm-runs right next to CN III • Pupillary-Sparing (pg. 194 in notes) o *Parasympathetic fibers run dorsally and peripherally within CN III

o Vasa nervorum lesion- spared pupillary  Because it supplies blood to CN III, so you lose everything; but spare papillary dilation and contraction because it’s part of parasympathetic function

CN IV • Nucleus at midbrain • Supplies superior oblique • Dysfunction: vertical diplopia CN VI • Nucleus at the pons • Most medial at the pontomedullary junction • Supplies lateral rectus • Dysfunction: horizontal diplopia (if you cover one eye, diplopia goes away) CN V • • • •

Nucleus in dorsal pons Know divisions of V1, V2, V3 (V1- crease of eye) Back of head innervated by C2 Muscles of mastication o Close Jaw  Temporalis  Masseter  Medial pterygoid o Open Jaw  Lateral pterygoid

CN VII • Nucleus at pons • Muscles of facial expression • Sound dampening • Lacrimation • Salivation • Taste of anterior 2/3 of tongue • Dysfunction: bells palsy o Ptosis: orbicularis oculi o Hyperacusis o Can’t curl their forhead/no wrinkles CN XII • Nucleus at medulla

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Dysfunction: tongue will deviate towards ipsilateral (LMN lesion)

CN XI • Sternocleidomastoid • Nucleus is cervical • 2 heads: o Sternomastoid- rotates head to contralateral side  Test by putting hand against patient’s face and having them turn their head o Cleidomastoid- tilts head forward and towards ipsilateral side • Trapezius o Lifting the arm higher when the deltoid is inhibited by the acromion 13. What are the contents of the cavernous sinus? What clinical presentation would be seen with a cavernous sinus thrombosis? • Contents: o CN III o CN IV o CN VI o CN V1 o Internal Carotid • Cavernous sinus thrombosis: o Blindness: compression of contral retinal artery o Chemosis: bloodshot sclera o Proptosis: eye bulges out 14. Remember: -Ptosis • CN III • CN VII • Sympathetics -Pupillary Dilation: • Sympathetics -Pupillary Constriction: • Parasympathetics via CN III -Midbrain: • Eye movements: CN III, CN IV • Decorticate posturing: fibers to red nucleus

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Impaired consciousness: reticular formation

-Pons: • Upper Pons: CN V • Lower Pons: CN VII, CN VIII • AICA infarct • SCA infarct • Pontine branches off basilar artery •

Findings associated with Pons lesions: o Bilateral babinski sign? o Generalized weakness (contralateral body) o Wrong way eyes: see eyes deviating toward the side of paralysis (ipsilateral horizontal gaze palsy)  Cortical seizure  Thalamic hemorrhage  Pons lesion • disrupt corticospinal fibers (get contralateral hemiplegia) • disrupt PPRF or abducens: ipsilateral gaze weakness o Decerebrate Posturing: due to lesion of reticulospinal tract (mid pons) o Impaired consciousness

-Medulla: • Nuclei for CN IX, X, XII, (XI-cervical, but travels back through there) • Symptoms: o CN VIII related (comes out at pontomedullary junction):  Vertigo  Ataxia  Nystagmus  Vomiting o Autonomic nervous system instability o Respiratory arrest o Hiccups • Causes: o Anterior spinal infarct (medial medullary syndrome) o Vertebral thrombosis or PICA (lateral medullary syndrome)