Tuberculosis of the Nose

Overview

• Cummings Otolaryngology Head and Neck Surgery

Who Is at Risk?

• Immunocompromised patients (including HIV-positive individuals)
• Healthcare workers
• Immigrants from endemic regions
• Older adults
• Those with HIV (HIV has driven a resurgence of TB and markedly increases risk of extrapulmonary forms)

Clinical Features

Symptoms & Signs

• Nasal obstruction and purulent rhinorrhea
• Epistaxis, crusting, nasal fissures
• Nodular thickening of the nasal mucosa, with or without ulcers (seen on nasal endoscopy)
• Lupus vulgaris - a painful, nodular tuberculoid lesion; this is the classic low-grade cutaneous form of TB and has been described in the nasal cavities
• Septal perforation - the cartilaginous septum is the most commonly involved structure
• With disease progression: saddle nose deformity can form

Paranasal Sinuses

• TB can also arise in the paranasal sinuses (frontal most commonly reported, also maxillary)
• Symptoms include headaches, nasal obstruction, discharge, diplopia, and proptosis depending on extent

Differential Diagnosis

• Syphilis
• Leprosy (Hansen disease)
• Rhinoscleroma (Klebsiella rhinoscleromatis)
• Wegener granulomatosis / GPA
• Cocaine-induced septal perforation
• NK/T cell lymphoma
• Leishmaniasis

Diagnosis

• Cummings Otolaryngology, Scott-Brown's Otorhinolaryngology

Treatment

• Prolonged multidrug anti-TB therapy is the mainstay - same regimen as pulmonary TB
• First-line drugs: Isoniazid + Rifampicin + Pyrazinamide (triple therapy)
• MDR-TB: Requires at least 3 drugs to which the isolate is susceptible; Directly Observed Treatment Strategy (DOTS) recommended, especially where compliance is a concern
• Nasal/pharyngeal TB requires no additional local treatment - systemic treatment resolves it

Key Points for the Nose Specifically

1. Most common site: Cartilaginous nasal septum
2. Classic lesion: Lupus vulgaris (painful nodular tuberculoid lesion)
3. End-stage: Saddle nose deformity from septal destruction
4. Septal perforation is a classic feature and is in the DDx for nasal septal perforations alongside syphilis, leprosy, cocaine use, and iatrogenic causes
5. TB of the nose is most often secondary to pulmonary TB (haematogenous or direct spread from infected sputum)

Physiology of the Vestibular System

Overview

1. Maintenance of balance (postural stability)
2. Maintenance of stable gaze (via the vestibulo-ocular reflex)

Anatomy of the Peripheral Vestibular System

• The SCCs are activated during rotational (angular) movements
• The otolith organs are activated during linear movements (including gravity/tilt)

Hair Cells - The Fundamental Transducers

Type I Hair Cells

• Flask-shaped
• Surrounded at the base by the afferent nerve terminal in a chalice-like fashion
• High tonic and dynamic electrical activity
• Largely stimulatory effect

Type II Hair Cells

• Cylindrical
• Surrounded by multiple nerve terminals
• Predominantly inhibitory effect

Structure of Hair Cells

• Each hair cell has 50-100 stereocilia + one long kinocilium projecting into the gelatinous matrix of the cupula (SCCs) or macula (otolith organs)
• The position of the kinocilium relative to the stereocilia gives each hair cell an intrinsic polarity

Transduction Mechanism

• Deflection of stereocilia toward kinocilium → increased Ca²+ influx at apex → neurotransmitter release → increased afferent firing
• Deflection away from kinocilium → decreased Ca²+ influx → neurotransmitter inhibition → decreased afferent firing

Semicircular Canals - Angular Acceleration Detection

Structure

• The hair cells of the SCCs are located in the crista ampullaris (the end organ within the ampullated portion of the membranous labyrinth)
• The cilia are embedded in a gelatinous mass called the cupula - it acts like a "hinged gate" between the vestibule and the canal

Mechanism

• Head rotation → endolymph (due to inertia) flows toward or away from the cupula → cupula bends → hair cell cilia deflected → nerve firing rate changes
• SCCs are paired structures:
  • Lateral canals are paired with each other
  • Left superior canal is functionally paired with right posterior canal (and vice versa)

Kinocilium Polarity

• Lateral SCC hair cells: kinocilia face toward the utricle (utriculopetal deflection = excitation)
• Superior and posterior SCC hair cells: kinocilia face away from the utricle (crus commune side; utriculofugal deflection = excitation)

Resting Firing Rate and Push-Pull Principle

• Hair cells fire at a baseline tonic rate even at rest
• During head rotation: one canal of the pair increases firing; the contralateral canal decreases firing
• This differential in firing rate is the signal the CNS uses to detect head movement direction and velocity
• Important limitation: Firing rate can increase without an upper limit, but can only decrease to zero - this asymmetry becomes clinically relevant at high velocities and after unilateral vestibular loss

Otolith Organs - Linear Acceleration & Gravity Detection

Structure

• Hair cells are located in the macula
  • Macula of the utricle: lies approximately in the plane of the horizontal canal (detects horizontal linear forces + gravity in upright position)
  • Macula of the saccule: lies approximately in the plane of the anterior canal (detects vertical linear forces)
• The cilia are embedded in the otolith membrane, which contains calcium carbonate crystals (otoliths/otoconia)
• Otoliths are denser than endolymph - this density difference is key to function

Mechanism

• Linear head acceleration (or gravity) → heavy otolith membrane lags behind the hair cells → cilia deflect → modulates afferent nerve activity
• The striola: a line that almost bisects the otolith membrane; hair cells on either side are oriented with their kinocilia facing toward or away from it - allows detection of acceleration in multiple directions

Role of Otolith Organs

• Play the greatest role in maintaining upright posture through detection of body/head tilt
• Provide gravity sensing and linear navigation signals

Vestibular Nerve

• Each vestibular nerve: ~25,000 bipolar neurons with cell bodies in the Scarpa ganglion (located within the internal auditory canal)
• Travels in the vestibular portion of CN VIII, contiguous to the cochlear portion

Central Vestibular System

Vestibular Nuclei (4 distinct nuclei at the pontomedullary junction)

Vestibulocerebellum

• Phylogenetically the oldest part of the cerebellum
• Includes: flocculus, nodulus, ventral uvula, ventral paraflocculus (flocculonodular lobe)
• Receives direct vestibular nerve projections
• Functions:
  • Conjugate eye movements, VOR, smooth pursuit
  • Holds image of a moving target on the fovea
  • Cancels VOR when needed (e.g., a figure skater spinning without getting dizzy)
  • Mediates vestibular compensation after unilateral loss

Neural Integrator

• Located in the reticular formation
• Responsible for the final velocity and position command for conjugate eye movements

Vestibulo-Ocular Reflex (VOR)

• Mechanism: Head movement detected by SCCs → vestibular nuclei → eye muscles produce movement equal and opposite to head movement
• Smooth pursuit is too slow to do this voluntarily - the VOR does it automatically
• Velocity/acceleration-dependent: the CNS needs velocity signals, not just directional signals
• Defect in VOR → "retinal slip" → reduced dynamic visual acuity → oscillopsia

VOR in Unilateral Vestibular Loss

• Sudden unilateral loss → affected side fires at zero; unaffected side fires at normal baseline
• CNS interprets this differential as head rotating toward the unaffected side
• VOR produces: slow phase toward the affected ear + fast phase (nystagmus) toward the unaffected ear
• Over time, the CNS compensates for changes in baseline firing, but VOR remains pathological at higher velocities

Types of Dizziness (Clinical Correlations)