Neuromyelitis optica spectrum disorder physical examination
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Julinka Auta Fernandes
Overview
- Neuromyelitis optica spectrum disorder (NMOSD) has no single pathognomonic physical examination finding. The examination is used to identify, localize, and document objective deficits caused by optic nerve, spinal cord, brainstem, diencephalic, or cerebral involvement.[1][2]
- A complete physical, neurologic, and ophthalmologic examination should be performed. The pattern and severity of abnormalities depend on the site, timing, and extent of the current attack and any residual deficits from previous attacks.[2]
- A normal or near-normal examination does not exclude NMOSD, particularly between attacks, after recovery, or when involvement is mild or subclinical.
Physical Examination
General appearance and vital signs
- There is no characteristic general appearance or vital-sign pattern specific to NMOSD.
- During a severe brainstem or high cervical spinal cord attack, assess respiratory rate and pattern, oxygen saturation, ability to speak in full sentences, cough strength, use of accessory muscles, and other signs of respiratory compromise.[2]
- Persistent observed hiccups or recurrent vomiting may accompany area postrema or medullary involvement; hydration status and signs of volume depletion should be assessed when vomiting is prolonged.[1][2]
Ophthalmologic examination
- Both eyes should be examined separately, even when visual impairment appears unilateral, because bilateral or clinically subtle optic nerve involvement may occur.[2]
- Assess habitually corrected high-contrast visual acuity in each eye. Reduced acuity may be severe during an acute optic neuritis attack; low-contrast visual acuity may reveal impairment when standard high-contrast acuity appears normal.[2][3]
- Examine color vision and red desaturation; impairment may be present in the affected eye.
- Test pupils for a relative afferent pupillary defect (RAPD) using the swinging-flashlight test. An RAPD supports asymmetric optic nerve dysfunction but may be absent when involvement is bilateral and symmetric.[2][3]
- Assess confrontation visual fields for an objective visual field defect.
- Perform fundoscopy. The optic disc may appear normal in retrobulbar optic neuritis or may show acute disc swelling; residual optic disc pallor or optic atrophy may be present after a previous attack.[2][3]
- Examine ocular alignment and extraocular movements for gaze palsy, ophthalmoplegia, diplopia-associated misalignment, or nystagmus indicating possible brainstem involvement.
Mental status and higher cortical function
- Assess level of consciousness, orientation, attention, memory, language, mood, and affect.
- Mental status is often preserved in isolated optic neuritis or myelitis. Objective altered alertness, hypersomnolence, cognitive impairment, encephalopathy, or postictal findings may occur with the less common diencephalic or cerebral presentations of NMOSD.[1][2]
Cranial nerve and brainstem examination
- Perform a complete cranial nerve examination, with particular attention to ocular motility, facial sensation, facial strength, speech, palatal movement, swallowing, and tongue movement.
- Objective abnormalities may include oculomotor disturbance, facial sensory loss, facial nerve palsy, dysarthria, dysphagia, nystagmus, or cranial-nerve-associated ataxia.[2]
- Examine for truncal, limb, and gait ataxia when brainstem or cerebellar pathway involvement is suspected.
Motor examination
- Assess muscle bulk, tone, and power in all four limbs using a reproducible grading method.
- Spinal cord involvement may produce objective weakness ranging from subtle monoparesis or paraparesis to severe paraplegia or tetraparesis. The distribution may be symmetric or asymmetric.[2]
- After the acute phase, an upper motor neuron pattern may include increased tone, spasticity, and pyramidal weakness below the level of the spinal cord lesion.
- During early severe myelitis, transient spinal shock may instead produce flaccid weakness and reduced tone.
- Observe for stimulus-induced or spontaneous painful tonic spasms during the examination when present.
Reflexes
- Examine deep tendon reflexes in the upper and lower limbs and assess plantar responses.
- Findings below a spinal cord lesion may include hyperreflexia, clonus, and extensor plantar responses. Reflexes may be reduced or absent transiently during acute spinal shock.
Sensory examination
- Examine light touch, pinprick, temperature, vibration, and joint-position sensation in the trunk and all limbs.
- Look for an objective spinal sensory level, which may help localize myelitis.
- Additional findings may include patchy or asymmetric sensory loss, impaired proprioception, and examination-evoked allodynia or hyperalgesia.[2]
Coordination and gait
- Test finger-to-nose and heel-to-shin coordination and assess for dysmetria.
- Evaluate stance and gait when safe, including ordinary, heel, toe, and tandem gait. Gait may be spastic, ataxic, sensory, weak, or untestable because of severe paresis.
- Document the need for assistance or a mobility aid and the patient's objective ambulatory capacity.
Autonomic and sacral examination
- In patients with suspected myelitis, objectively assess for urinary retention or incontinence and bowel dysfunction; abdominal examination may reveal suprapubic fullness from a distended bladder.[2]
- When clinically indicated, perform a focused sacral neurologic examination, including perianal sensation and anal sphincter tone.
- Autonomic findings document spinal cord dysfunction but are not specific for NMOSD.
Repeat examination and documentation
- Record baseline abnormalities and their laterality and severity. Repeat neurologic and ophthalmologic examinations if new findings develop, because optic nerve, spinal cord, brainstem, or cerebral involvement may appear sequentially during the same attack.[2]
- In an initially unilateral optic neuritis attack, repeat examination of both eyes is important because contralateral involvement may emerge after a delay.[2]
- Physical examination findings support anatomic localization and measurement of attack severity; they do not independently confirm or exclude NMOSD. Current consensus diagnosis requires integration with the appropriate diagnostic evaluation.[1][4]
References
- ↑ 1.0 1.1 1.2 1.3 Wingerchuk DM, Banwell B, Bennett JL, et al. International consensus diagnostic criteria for neuromyelitis optica spectrum disorders. Neurology. 2015;85(2):177-189. doi:10.1212/WNL.0000000000001729. PMID: 26092914; PMCID: PMC4515040.
- ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 Jarius S, Aktas O, Ayzenberg I, et al.; Neuromyelitis Optica Study Group. Update on the diagnosis and treatment of neuromyelitis optica spectrum disorders—revised recommendations of the Neuromyelitis Optica Study Group. Part I: Diagnosis and differential diagnosis. Journal of Neurology. 2023;270(7):3341-3368. doi:10.1007/s00415-023-11634-0. PMID: 37022481; PMCID: PMC10267280.
- ↑ 3.0 3.1 3.2 Petzold A, Fraser CL, Abegg M, et al. Diagnosis and classification of optic neuritis. The Lancet Neurology. 2022;21(12):1120-1134. doi:10.1016/S1474-4422(22)00200-9. PMID: 36179757.
- ↑ Yamout B, Gouider R, Al-Roughani R, et al. Consensus recommendations for the diagnosis and treatment of neuromyelitis optica spectrum disorders: The Middle East and North Africa Committee for Treatment and Research in Multiple Sclerosis guidelines. CNS Drugs. 2026;40(3):283-303. doi:10.1007/s40263-025-01260-x. PMID: 41591715.