Normal Tension Glaucoma

May be a distinct phenotype from POAG: local vascular dysregulation at the optic disc may play a role. Clinical features are as for POAG

Specific characteristics of NTG:

• Increased disc haemorrhages
• More prominent peripapillary atrophy
• More prominent disc notching
• More disc sloping
• Larger disc size
• Deeper field defects
• Field defects closer to fixation

Associations

• Migraine (central vascular dysregulation)
• Raynaud’s (peripheral)
• Hypotension especially with nocturnal dipping
• OSA

Risk factors

• Age
• Ethnicity: commoner in Japan
• F>M

Tests

• Pachymetry is important as may suggest under-reading of IOP

• IOP phasing: regular IOP checks over an extended period of the day +/- provocative tests (eg. drinking water)

• Gonioscopy

• MRI with fine-cut to assess the anterior visual pathway with gadolinium enhancement

  • Especially if positive visual symptoms: reduced VA/colour vision, RAPD, disc pallor or VF defects observing the vertical midline

• Exclude other optic neuropathies: FBC, B12, folate, ESR, syphilis-serology, ACE, ANA, ANCA, CRP, LHON screen, CXR

• Ambulatory BP monitoring especially if on beta-blockers

Collaborative Normal Tension Glaucoma study

• An IOP reduction of >30% slows the rate of field loss

• Even without treatment, 50% of NTG patients do not progress at 5 years

• Risk factors for progression

  • Female
  • Migraine
  • Disc haemorrhage at diagnosis

Management

As for POAG

• Prostaglandin analogues may be more important in NTG to facilitate better nocturnal control
• Systemic (and topical) beta-blockers may actually reduced nocturnal blood flow and therefore optic nerve perfusion so may be less preferable