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Cranial nerves

Cranial nerves. Trigeminal nerve. Trigeminal nerve. V: Trigeminal (3 nerves in 1!) . V1. Ophthalmic Exits with eye muscle group (superior orbital fissure, through orbit to superior orbital notch/foramina) Sensory to forehead, nasal cavity V2. Maxillary

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Cranial nerves

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  1. Cranial nerves

  2. Trigeminal nerve

  3. Trigeminal nerve

  4. V: Trigeminal (3 nerves in 1!) • V1. Ophthalmic • Exits with eye muscle group (superior orbital fissure, through orbit to superior orbital notch/foramina) • Sensory to forehead, nasal cavity • V2. Maxillary • Exits foramen rotundum through the wall of maxillary sinus to inferior orbital foramina) • Sensory to cheek, upper lip, teeth, nasal cavity • V3. Mandibular • Exits foramen ovale to mandibular foramen to mental foramen • Motor to jaw muscles--Masseter, temporalis, pterygoids, digastric • Sensory to chin • Sensory to tongue

  5. Human Anatomy, Frolich, Head/Neck IV: Cranial Nerves

  6. Trigeminal neuralgia

  7. TRIGEMINAL NEURALGIA(Tic Douloureux) • A disorder of the trigeminal nerve producing bursts of excruciating, lancinating pain, lasting between seconds and 2 min, along the distribution of one or more of its sensory divisions, most often the maxillary. • vascular loops compressing the trigeminal nerve root where it enters the brainstem • usually adults • trigger point or by activity (eg, chewing or brushing the teeth). • Although each bout of intense pain is brief, successive bouts may be incapacitating.

  8. TRIGEMINAL NEURALGIADifferential diagnosis • Neoplasm • Vascular malformation of the brain stem, • Vascular insult, • Multiple sclerosis (especially in a younger patient). • Postherpetic pain • typical antecedent rash, scarring, and predilection for the ophthalmic division. • Sjögren's syndrome or RA, (with a sensory deficit that is often perioral and nasal). • Migraine may produce atypical facial pain, with normal examination results, but the pain is more prolonged and is burning or throbbing.

  9. Treatment • carbamazepine (Tegretol®), fenitoin (Dilantin®), oxcarbazepine (Trileptal®), gabapentin (Neurontin®). • Use of Baclofen (Lioresal®) may increase efficiency • Neurontin®, (gabapentin), Lyrica ® (pregabalin) – lower rates of adverse effects

  10. Surgical treatment • Percutaneous risotomy (glycerol injection, baloon compression, radiofrequency risotomy) • Peripheral blocks, section, avulsion • Microsurgery risotomy • Gammaknife radiosurgery

  11. Trigeminal paralysis • Weakness, hipotonia and atrophies of the maseter and temporal muscles • Jaw deviates towards affected side upon closure of the mouth, • can not perform jaw lateral movements to the affected side

  12. Facial nerve

  13. Bell's Palsy • Unilateral facial paralysis of sudden onset and unknown cause. • swelling of the nerve due to immune or viral disease, with ischemia and compression of the facial nerve in its course through the temporal bone. • Pain behind the ear may precede facial weakness. • Weakness develops within hours, sometimes to complete paralysis. • The patient may complain of a numb or heavy feeling in the face, but no sensory loss is demonstrable. • A proximal lesion may affect salivation, taste, and lacrimation and may cause hyperacusis.

  14. Differential Diagnosis • Disorders of the facial nerve or its nucleus, chiefly geniculate herpes (Ramsay Hunt's syndrome), • Middle ear or mastoid infections, • Sarcoidosis, • Lyme disease, • Petrous bone fractures, • Carcinomatous or leukemic nerve invasion, • Chronic meningeal infections, and • Cerebellopontine angle or glomus jugulare tumors. • Temporal bone fracture

  15. Bell’s Palsy • Treatment • Oral antivirals - Acyclovir - 10mg/kg (500mg) q8hrs x 7 days • Corticosteroid • Prednisone taper 1mg / kg / day for 10 days • methylprednisolone • Eye protection - lacrilube • Follow progression with serial exams • Facial nerve decompression • Performed before irreversible injury to the endoneural tubules occurs (two weeks), will allow for axonal regeneration to occur

  16. What if the facial paralysis doesn’t resolve? • End-to-End Anastomosis • Cable Nerve Graft • Hypoglossa-Facial Nerve Anastomosis (Crossover or Jump Graft) • Muscle transposition (Gracilis) • Static Suspension (Gortex, Threads)

  17. Complications • Keratitis • Emotional/Social Issues • Synkinesis

  18. Ramsay Hunt Syndrome

  19. Central vs peripheral paralysis Weakness of the entire half of the face distinguishes Bell's palsy from supranuclear lesions (eg, stroke, cerebral tumor), in which the weakness is partial, affecting the frontalis and orbicularis oculi less than the muscles in the lower part of the face

  20. Oculomotricity

  21. Centre for saccadic (fast) voluntary or reflex movements. Activation leads to fast deviation of eyes towards opposite side Centre for slow following motions. Activation leads to slow deviation of eyes Fronto-mezencephalic pathway Occipito-mesencephalic pathway III rd nerve nucleus (both pathways end in the oculomotor nerves nuclei) Medial longitudinal bundle Reticular paramedian pontine formation – centre for lateral

  22. Ocular motricity

  23. 3rd nerve - Oculomotor nerve • Somatic fibers: 4 out of the 6 extraoculary muscles and also the elevator of the upper lid • Control of the eye movements during following or fixation movements • Visceral fibers: parasympathetic fibers for the pupilar constrictor and ciliary muscles • Involved in the accomodation pupilary reflexes

  24. 3rd nerve - Oculomotor nerve

  25. VI th nerveabducens

  26. 6th nerve – Abducens nerve

  27. Abducens nerve palsy (left side)

  28. 4th nerve – Trochlear nerve

  29. Trochlear nerve • Contraction of the superior oblique muscle generates depression, internal rotation and abduction of the eye • Lesions of the 4th nervegenerate • External rotation (unbalanced action of inferior oblique muscle) • Diplopia (vertical) • Problems with looking down, especially for the eye that looks internally – problems with descending stairs • Compensatory rotation of the head • Due to its long way around the brainstem, the 4th nerve is prone to lesions in head trauma • Special features: • Trasaturi speciale: • Theonly cranial nerve that emerges on the posterior side of the midbrain • All fibers from the lower motor neuron cross • It has the longest intracranian passage • Contains the least axons compared to the other cranian nerves

  30. trohlear • normal • Superior oblique muscle palsy

  31. joint deviation of the eyes and head

  32. Internuclear palsies

  33. Miasthenia gravis

  34. The Anatomy of the Neuromuscular Junction • Motor neurone terminates as a bouton or pre-synaptic nerve terminal separated from the muscle by a thin synaptic cleft (Motor endplate) • The blood nerve barrier is relatively deficient at the NMJ • Nerve and muscle are kept in close proximity by bridging protein (laminin), with release zones and the crests of post synaptic folds aligned • The skeletal neuromuscular junction is the most studied and best understood synapse

  35. Healthy Neuromuscular Junction

  36. The Physiology of Neuromuscular transmission • Neuronal Action potential invades the pre-synaptic nerve terminal • Depolarisation triggers opening of VGCCs • Calcium influx triggers quantal release of ACh • ACh binds to post synaptic nAChRs • Ca and Na ions influx through nAChR triggering muscle membrane depolarisation via VGSCs- CMAP and muscle contraction

  37. Spontaneous and Nerve Evoked Endplate Responses

  38. Myasthenia Gravis (MG) • MG is the most common disorder of neuromuscular transmission • Incidence 2-6 per 106 , prevalence 40 per 106 population • MG is an acquired autoimmune disease characterised by the formation of anti- nAChR antibodies • MG is common in young women, and older men • MG is characterized by fluctuating and fatigable weakness • Weakness may be limited to a few muscles, such as the extraocular muscles, bulbar, limb or be generalised in fashion • As the weakness is often worse with activity and improved by rest, • it is often worse in the evening

  39. Myasthenia Gravis (MG) • Ocular features: ptosis, diplopia, ophthalmoplegia • Facial weakness esp ob oculi and oris (snarl) • Bulbar weakness: nasal speech, reduced gag, swallowing • problems, aspiration (silent), weak neck (dropped) • Limb weakness: proximal, fatiguable • Reflexes: normal • Respiratory weakness: diaphragm and intercostal Fenomenul de oboseală (ptoză) în MG

  40. Myasthenia Gravis (MG) • MG is a defect of neuromuscular transmission with • reduced efficacy of Acetyl Choline at the post synaptic motor endplate due to pathogenic antibodies which • Block the nAChR, • Down regulate the nAChR • & cause complement dependent destruction of the motor endplate

  41. Myasthenia Gravis (MG) • The immunopathogenesis of MG is unclear but involves • Genetic factors (HLA B8) • Thymus • Vast majority of young onset cases are autoimmune and associated with thymic hyperplasia • Around 10% of patients with MG, often older patients) have an associated thymic tumour (oft striated muscle Abs) • Seronegative (10% gen, 50% OMG) • Neonatal MG

  42. Tensilon test – before and after Single fiber EMG – normal Single fiber EMG – increased jitter Myasthenia Gravis (MG) • Diagnosis • Typical clinical picture • Detection of anti-AChR antibodies in serum (90%) • Positive Tensilon test (atropine) • Repeptitive nerve stimulation at low frequency leads to a decrement in compound muscle action potential amplitude

  43. Repetitive Nerve Stimulation (Supramaximal 2Hz)

  44. Myasthenia Gravis (MG) • Treatment • Symptomatic (pyridostigmine oft with probatheline) • Thymectomy • Hyperplasia (trans-sternal approach), • Thymoma (locally invasive) • Immunotherapy • steroids, and other agents including Azathioprine • plasma exchange, • IVIG

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