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Lanning B. KLine, MD anD RoD FoRoozan, MD I. AnAtomIcAl consIderAtIons (FIgure 12-1)
The trigeminal nerve is a mixed nerve 1. Motor—ipsilateral muscles of mastication (masseter, temporalis, ptery-goids) Sensory portion of trigeminal nerve extends from the midbrain to the upper cervical cord Mesencephalic (rostral) nucleus—proprioception and deep sensation from tendons and muscles of mastication Extends from pons to upper cervical cord Divided into segments that correspond to dermatomes that are concentric around the mouth The trigeminal nerve supplies sensation to the ipsilateral side of the face via three branchesa. V1—Ophthalmic division: frontal, lacrimal, and nasociliary b. V2—Maxillary division: cheek and lower eyelid c. V3—Mandibular division: area of mandible (but not angle of Motor nucleus lies in pons medially to main sensory nucleus and axons travel with mandibular (V3) division Figure 12-1. Figure caption will come
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Three divisions of trigeminal nerve converge at trigeminal (gasserian) gan-glion, which lies in Meckel’s cave of temporal bone Fibers then travel through main sensory root to brainstem II. oculoFAcIAl hypesthesIA (see FIgure 12-1)
Distribution of facial numbness or paresthesias helps determine central or peripheral origin 1. Concentric perioral numbness/paresthesia—central (nuclear) origin (eg, isch-emia, demyelination) Band of numbness/paresthesia—peripheral origin (ie, V1, V2, V3) Such somatotopic hypesthesia (eg, V1 only, or V2 and V3 with sparing of V1) suggests that the lesion is more likely to be in the middle cranial fossa (cavern-ous sinus) or orbit B. Differential diagnosis of diminished sensation in the trigeminal distribution Perineural spread of skin carcinoma (see Chapter 12, III, B, 5) Neoplasm, foremen rotundum, sphenopterygoid fossa Involvement of mental nerve (terminal branch of inferior alveolar nerve) Frequently due to systemic cancer: breast, lymphoproliferative disorders iii. Contrast—enhanced imaging (computed tomography [CT] or magnetic resonance imaging [MRI]) of head including skull base and mandible Brainstem lesions (dissociated sensory loss) III. oculoFAcIAl pAIn
Differential diagnosis of relatively common entities associated with ocular and facial pain on the basis of clinical findings 1. Most commonly with an abnormal anterior segment examination i. Chronic ocular hypoxia, carotid occlusive disease Often with a normal anterior segment examinationi. Glaucoma, including intermittent angle-closure glaucoma Can occur with or without ophthalmic findings a. Primary headaches syndromes including migraine and cluster headaches Herpes zoster—nasociliary nerve involvement indicated by vesicular eruption on side or tip of nose (Hutchison’s sign) May be followed by postherpetic neuralgia Referred (dural) pain, including occipital infarction Cavernous sinus syndromes (see Chapter 7)i. Tumorsii. m. Elevated intracranial pressure and idiopathic intracranial hypertensionn. Pain with medullary lesions (eg, Wallenberg syndrome) Occipital neuralgia can sometimes be confused with other causes of head and facial pain Any intracranial process irritating the dural sensory fibers, which may be supplied by recurrent branches of V nerve Neck pain (eg, from osteoarthritis in the cervical spine) may be referred to the eye because of the cervical sensory fibers traveling with the trigeminal fibers of the spinal tract of V, which extends to C-2 level Trigeminal neuralgia (tic douloureux) a. Paroxysmal pain in the distribution of one or more of the divisions of V (V3 > V2 > V1) Recurring, lancinating, “lightning” hemifacial pain lasting 20 to 30 seconds Pain may be so intense that the facial muscles contract and distort the face during an attack. Frequently “triggered” by touching certain areas of the face or scalp; asymptomatic or mild headache between episodes No neurologic deficits (including normal corneal reflex) Neuralgia of more persistent nature and associated with neurologic deficits may resolve from compressive, demyelinative, or inflammatory lesion of the V nerve Anticonvulsants carbamazepine and gabapentin Microvascular decompression of aberrant vessel at V nerve root entry zone Trigeminal ganglion destruction or stereotactic radiosurgery Pain of herpes zoster is described as severe, burning, aching in quality Pain occurs over distribution of a dermatome of cranial nerve, usually V1, although it may involve the facial nerve (external ear) with ipsilateral facial palsy (Ramsay Hunt syndrome) Pain often precedes onset of typical rash by 4 to 7 days Pain usually regresses within 1 to 2 weeks, but may persist for months or years: post-herpetic neuralgia Patients typically describe dysesthesias as “crawling” and “prickly” sensations Treatment frequently is difficult but may includei. Gabapentinii. Pregabaliniii. Tricyclic antidepressantsiv. Treatment of herpes zoster with antiviral therapy may decrease the risk of postherpetic neuralgia A vaccine for herpes zoster has been helpful in limiting the morbidity of postherpetic neuralgia V nerve distribution pain with ipsilateral Horner’s syndrome Almost exclusively in middle-aged or elderly male patients May be caused by migrainous dilation of the internal carotid artery with compression of the V nerve and sympathetic plexus in the middle cranial fossa If the pain is persistent (not of migrainous episodic nature) or if associated with cranial nerve palsy, then suspect a middle fossa tumor, aneurysm, or internal carotid artery dissection Initial involvement often limited to single nerve branch (especially infra-orbital) but proximal spread leads to cavernous sinus involvement Often signals recurrence of previously treated tumor, the treatment of which may be forgotten by the patient Frequently due to squamous cell carcinoma of the face or oropharyngeal mucosa Diagnosis established with contrast-enhanced MRI BookMongini F. Headache and Facial Pain. Stuttgart, Germany: Thieme; 1999.
Chapters Glaser JS. Neuro-Ophthalmology. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1999:64-70. Liu GT. The trigeminal nerve and its central connections. In: Miller NR, Newman NJ, eds. Walsh and Hoyt’s Clinical Neuro-Ophthalmology. 6th ed. Vol 1. Philadelphia, PA: Lippincott Williams & Wilkins; 2005:1233-1274. Martin TJ, Corbett JJ. Neuro-Ophthalmology—The Requisites. St Louis, MO: Mosby; 2000:223-232. Van Stavern GP. Headache and facial pain. In: Miller NR, Newman NJ, eds. Walsh and Hoyt’s Clinical Neuro-Ophthalmology. 6th ed. Vol 1. Philadelphia, PA: Lippincott Williams & Wilkins; 2005:12751311. Articles Biousse V, Toubol PJ, D’Anglejan–Chatillon J, et al. Ophthalmologic manifestation of internal carotid artery dissection. Am J Ophthalmol. 1998;126:565-577. Clouston PD, Sharpe DM, Corbett AJ, et al. Perineural spread of cutaneous head and neck cancer: its orbital and central neurologic complications. Arch Neurol. 1990;47:73-77. Fazzone HE, Lefton DR, Kupersmith MJ. Optic neuritis, correlation of pain and magnetic resoance imag- ing. Ophthalmology. 2003;110:1646-1649.
Harooni H, Golnik KC, Geddie B, et al. Diagnostic yield for neuroimaging in patients with unilateral eye or facial pain. Can J Ophthalmol. 2005;40:759-763.
Lee AG, Beaver HA, Brazis PW. Painful ophthalmologic disorders and eye pain for the neurologist. Neurol Levin LA, Lessell S. Pain: a neuro-ophthalmic perspective. Arch Ophthalmol. 2003;121:1633. Pavan-Langston D. Herpes zoster: antivirals and pain management. Ophthalmology. 2008;115(2 Prasad S, Galetta S. Trigeminal neuralgia; historical notes and current concepts. Neurologist. 2009;15:87-94.
Ringeisen AL, Harrison AR, Lee MS. Ocular and orbital pain for the headache specialist. Curr Neurol Neurosci Rep. 2011;11:156-163.

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