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Trigeminal Nerve (CN V) Examination

Anatomy Overview

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Examination Components

1. Motor Function

• Masseter and temporalis: Ask the patient to clench their teeth firmly. Palpate both muscles simultaneously - compare bulk and strength side-to-side.
• Pterygoids (jaw opening): Ask the patient to open their mouth. In unilateral pterygoid weakness, the jaw deviates toward the weak (affected) side due to the unopposed action of the contralateral pterygoid.
• Lateral pterygoid (jaw protrusion): Ask the patient to push the jaw forward and side to side; resist the movement to assess strength.

Note: The upper motor neuron control to the trigeminal motor nucleus is predominantly bilateral, so a unilateral corticobulbar lesion usually causes no jaw weakness. However, bilateral upper motor neuron lesions (e.g., ALS, diffuse white matter disease) cause a brisk jaw jerk and possible spastic jaw. - Neuroanatomy through Clinical Cases, 3e

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2. Sensory Function

• V1: Forehead (above eyebrows)
• V2: Cheek (malar eminence / below the eye)
• V3: Chin and lower jaw

• Mucous membranes of nose, mouth, and paranasal sinuses
• Anterior 2/3 of tongue (general sensation, not taste - taste is CN VII)
• Conjunctiva

Testing of two sensory modalities derived from different anatomic pathways (e.g., light touch and temperature) is sufficient for a screening examination. - Harrison's Principles of Internal Medicine, 22e

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3. Corneal Reflex

• Afferent limb: Ophthalmic division (V1) → chief sensory nucleus + spinal trigeminal nucleus
• Efferent limb: Facial nerve (CN VII) → orbicularis oculi → eye closure

• Direct reflex: closure of the ipsilateral eye
• Consensual reflex: closure of the contralateral eye

Lesions of the trigeminal sensory pathways, the facial nerve, or their connections causes a decreased corneal reflex in the ipsilateral eye. - Neuroanatomy through Clinical Cases, 3e

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4. Jaw Jerk Reflex (Masseter Reflex)

• Afferent limb: Ia fibers in the mandibular division (V3) → mesencephalic trigeminal nucleus
• Efferent limb: Motor nucleus of CN V → masseter and temporalis

In normal individuals, the jaw jerk reflex is minimal or absent. In bilateral upper motor neuron lesions, the jaw jerk reflex may be brisk. - Neuroanatomy through Clinical Cases, 3e

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5. Sneezing Reflex (Additional)

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Interpretation Summary

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Clinical Localization Pearls

• Gasserian ganglion lesion (e.g., herpes zoster, schwannoma): all three divisions affected + motor weakness
• Cavernous sinus lesion: V1 and V2 affected (V3 exits separately at foramen ovale and is spared)
• Brainstem lesion (spinal trigeminal tract): ipsilateral facial pain/temperature loss with contralateral body sensory loss = lateral medullary (Wallenberg) syndrome
• Supranuclear lesion: unilateral cortical lesion usually spares jaw movement (bilateral representation); bilateral lesions cause pseudobulbar palsy with brisk jaw jerk
• Mental nerve (branch of V3) neuropathy presenting as isolated chin/lower lip numbness is a red flag for mandibular metastasis

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• Harrison's Principles of Internal Medicine, 22e
• Adams and Victor's Principles of Neurology, 12e
• Neuroanatomy through Clinical Cases, 3e
• Localization in Clinical Neurology, 8e
• S. Das Manual of Clinical Surgery, 13e

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Transverse Myelitis - Complete Notes

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1. Definition

• Motor deficits (paraparesis/paraplegia)
• Sensory deficits (with a sensory level)
• Autonomic dysfunction (bladder, bowel, sexual)

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2. Epidemiology

• Incidence: approximately 1-8 per million per year
• Bimodal age distribution: peaks at 10-19 years and 30-39 years
• No strong sex predilection in idiopathic TM, but NMOSD-related TM is more common in women
• Thoracic cord is most commonly affected (60-70% of cases); cervical cord involvement is less common

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3. Etiology and Classification

Primary Categories:

Key Subtypes:

• Signal abnormality extending >3 vertebral segments on MRI
• Hallmark of NMOSD (NMO spectrum disorder)
• Associated with anti-AQP4 (aquaporin-4) antibodies

• Signal abnormality extending <2 vertebral segments
• More characteristic of MS involvement

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4. Pathophysiology

• Underlying mechanism varies by etiology
• Common pathway: inflammatory infiltration of the spinal cord → demyelination ± axonal damage → disruption of motor, sensory, and autonomic tracts
• In NMOSD: antibodies target aquaporin-4 water channels on astrocytic end-feet → astrocyte destruction → secondary oligodendrocyte death and demyelination
• In post-infectious TM: molecular mimicry or bystander activation of immune response
• Lesions in TM tend to involve >2/3 of the cross-sectional area of the cord (vs. MS lesions which involve <1/2)

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5. Clinical Features

Onset

• Usually rapid: 66% reach maximal deficit within 24 hours; may progress over days to weeks
• Often preceded by back pain or radicular pain at the level of the lesion
• Low-grade fever may be present (post-infectious)

Classic Triad:

A. Motor Deficits

• Acute phase (spinal shock): flaccid paralysis, hypotonia, hyporeflexia below the lesion
• Subacute/chronic phase: spastic paraplegia, hyperreflexia, clonus, bilateral Babinski signs
• Loss of superficial abdominal and cremasteric reflexes
• Extension posturing with incomplete/high lesions; flexion posturing with complete lower cord lesions

B. Sensory Deficits

• Sensory level on the trunk - most valuable localizing sign
• All modalities impaired below the lesion
• Band-like radicular pain or paresthesias at the level of the lesion
• With extramedullary compression, sensory level may be several segments below the actual lesion (due to somatotopic organization of spinothalamic tract - sacral fibers are most superficial)

C. Autonomic Dysfunction

• Bladder: urinary retention, overflow incontinence, or urgency
• Bowel: constipation or incontinence
• Sexual dysfunction
• Cardiovascular: hypo- or hypertension, brady- or tachycardia (in high cervical lesions)

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6. Investigations

A. MRI Spine (with and without gadolinium) - Investigation of Choice

• T2-weighted: intramedullary high signal (hyperintensity) with cord swelling
• Gadolinium enhancement: present in active inflammation
• TM lesions: involve >2/3 of cord cross-section on axial views
• LETM (>3 segments): points toward NMOSD
• Short lesion (<2 segments, peripheral, dorsal): points toward MS

If MS is suspected: also obtain brain MRI - cerebral white matter lesions support diagnosis of MS even if asymptomatic.

B. CSF Analysis (Lumbar Puncture)

• Normal in 40% of cases
• Abnormal (60%): mild lymphocytic pleocytosis + elevated protein
• Oligoclonal bands (IgG): suggest MS
• CSF is not diagnostic but helps exclude infection and support inflammation

C. Blood Tests

• Anti-AQP4 (anti-aquaporin-4) antibodies / NMO-IgG - key test for NMOSD
• Anti-MOG (myelin oligodendrocyte glycoprotein) antibodies - seronegative NMOSD variant
• ANA, anti-dsDNA, antiphospholipid antibodies - screen for SLE and autoimmune CTD
• Vitamin B12, folate
• Infectious workup (viral serology, TB, Lyme, syphilis) as clinically indicated

D. Other

• Somatosensory and motor evoked potentials: demonstrate conduction delay across the lesion
• Nerve conduction studies / EMG: to rule out peripheral nerve or neuromuscular disease

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7. Diagnostic Criteria (Transverse Myelitis Consortium Working Group)

1. Sensory, motor, or autonomic dysfunction attributable to the spinal cord
2. Bilateral signs/symptoms (not necessarily symmetrical)
3. Clearly defined sensory level
4. Inflammation demonstrated by CSF pleocytosis, elevated IgG index, or MRI gadolinium enhancement (if none present, repeat MRI in 2-7 days)
5. Nadir between 4 hours and 21 days of onset

• History of prior radiation to spine
• Clear arterial distribution of deficit (vascular)
• Extramedullary compressive etiology on MRI
• Abnormal flow voids suggesting AV malformation
• Connective tissue disease serologically negative (does not exclude)

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8. Differential Diagnosis

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9. Management

A. Acute Phase (First-line)

• Methylprednisolone 1 g IV daily for 3-5 days
• Mechanism: reduces inflammation, stabilizes blood-brain/spinal cord barrier
• Standard of care especially for NMOSD-related TM
• Evidence is limited for idiopathic TM but widely used

B. Second-line (Steroid-refractory)

• 5-7 exchanges over 10-14 days
• Used when patients fail to improve with steroids
• Removes pathogenic antibodies (especially useful in AQP4-Ab positive NMOSD)

• Used in selected cases, especially post-infectious or MOG-Ab associated TM

C. Long-term / Preventive (NMOSD)

• Azathioprine (with or without oral prednisolone)
• Mycophenolate mofetil
• Rituximab (anti-CD20)
• Newer biologics: Eculizumab, Inebilizumab, Satralizumab - FDA-approved for AQP4-Ab+ NMOSD

D. Symptomatic and Supportive

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10. Prognosis

• Clinical course is highly variable
• Most patients with idiopathic TM show at least partial recovery beginning within 1-3 months
• Maximal improvement usually by 3-6 months

Outcome breakdown (idiopathic TM):

Poor Prognostic Factors:

• Rapid onset to nadir (<24 hours)
• Severe deficits at nadir (complete paraplegia)
• Back pain at onset
• Spinal shock at presentation
• NMOSD (high relapse rate, cumulative disability)
• AQP4-Ab positivity

Risk of MS:

• Up to one-third of patients do not have evidence of disseminated demyelination at 5 years (monophasic course)
• Those with brain MRI lesions + oligoclonal bands at presentation have higher risk of converting to MS
• Risk of MS progression after an isolated TM episode is similar to that after a first episode of optic neuritis

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11. TM vs. MS vs. NMOSD - Comparison Table

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• Rosen's Emergency Medicine, 10e
• Adams and Victor's Principles of Neurology, 12e
• Bradley and Daroff's Neurology in Clinical Practice
• Localization in Clinical Neurology, 8e
• Grainger & Allison's Diagnostic Radiology