Autoimmune Encephalitis physical examination
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Julinka Auta Fernandes
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Autoimmune Encephalitis Microchapters |
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Differentiating Autoimmune Encephalitis from Other Conditions |
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Diagnosis |
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Autoimmune Encephalitis On the Web |
Overview
Physical examination in autoimmune encephalitis may reveal altered mental status, impaired memory, abnormal behavior, speech disturbance, seizures, or a movement disorder. Severe presentations may include reduced consciousness, autonomic instability, and respiratory compromise. Findings vary with the clinical syndrome, age, disease stage, and medication exposure.[1]
No single physical finding establishes an autoimmune cause. The absence of fever or focal neurological signs does not exclude encephalitis.[2]
Physical Examination
Appearance of the Patient
- Autoimmune encephalitis may be associated with agitation, disinhibition, emotional lability, reduced spontaneous interaction, or lethargy.
- Severe disease may produce stupor or coma. Level of consciousness can be recorded using the Glasgow Coma Scale, with medication effects and barriers to verbal responses documented.
- Mutism, immobility, abnormal posturing, or negativism may accompany catatonia. These findings require interpretation within the broader neurological and psychiatric presentation.[3][2]
Vital Signs
Autoimmune encephalitis may cause autonomic and respiratory abnormalities, particularly in severe disease. Vital signs may also reflect infection, seizures, medications, or another concurrent illness.[2]
| Parameter | Potential finding |
|---|---|
| Temperature | Fever or temperature instability; fever is not required for the diagnosis. |
| Pulse | Tachycardia, bradycardia, marked heart-rate fluctuations, or an irregular pulse. |
| Blood pressure | Hypertension, hypotension, or substantial fluctuations accompanying autonomic dysfunction. |
| Respiratory rate and pattern | Abnormally slow, shallow, or irregular breathing, including central hypoventilation. |
| Oxygen saturation | Reduced saturation when respiratory compromise is present. |
Skin
- Autoimmune encephalitis with autonomic dysfunction may be accompanied by diaphoresis.
- A rash, injection marks, or other exposure-related findings may suggest an infectious, toxic, or systemic alternative rather than a characteristic autoimmune encephalitis skin lesion.[2]
Head, Eyes, Ears, Nose, and Throat (HEENT)
- Autoimmune encephalitis may produce conspicuous repetitive movements of the lips, tongue, jaw, or face as part of an orofacial movement disorder.
- Nystagmus, impaired eye movements, or ophthalmoplegia may occur with selected brainstem or cerebellar presentations; these are not universal findings.[4][3]
Neck
- Autoimmune encephalitis assessment may reveal neck stiffness or other evidence of meningism. Meningeal signs are insensitive, and their presence does not distinguish an autoimmune from an infectious cause.
- Lymphadenopathy, when present, may provide a clue to an associated systemic illness or neoplasm.[2][1]
Lungs
- Autoimmune encephalitis can be accompanied by central hypoventilation, irregular respiratory effort, or respiratory failure in severe presentations.
- Abnormal respiratory findings may also reflect aspiration or infection complicating reduced consciousness or seizures.[2]
Heart
- Autoimmune encephalitis with dysautonomia may produce tachycardia, bradycardia, or an irregular pulse.
- Cardiovascular instability is a marker of potentially severe illness and requires prompt assessment.[3]
Abdomen and Genitourinary Examination
- Autoimmune encephalitis may be associated with an underlying neoplasm. A palpable abdominal, pelvic, or testicular abnormality, if present, can direct further evaluation.
- Absence of a palpable mass does not exclude an occult tumor or replace appropriate tumor screening.[1]
Extremities
- Autoimmune encephalitis may be associated with limb dystonia, abnormal posturing, tremor, or myoclonus.
- Visible fasciculations or myokymia, reflecting spontaneous muscle overactivity, can accompany contactin-associated protein-like 2 (CASPR2) antibody-associated disease. The broader CASPR2 spectrum includes peripheral nerve involvement as well as encephalitis.[5]
Neuromuscular
Mental status and cognition
Autoimmune encephalitis may produce impaired attention, disorientation, poor recent recall, executive dysfunction, agitation, or reduced awareness. Cognitive and behavioral abnormalities may dominate even when obvious focal motor deficits are absent.[1]
Speech and language
Autoimmune encephalitis may cause reduced verbal output, pressured speech, mutism, or aphasia. Dysarthria or impaired swallowing associated with dysphagia may accompany selected brainstem presentations.[3][4]
Movement abnormalities
Autoimmune encephalitis can produce mixed movement disorders, including:
- Orofacial dyskinesias and repetitive stereotyped movements.
- Dystonia or sustained abnormal posturing.
- Chorea, myoclonus, or tremor.
- Rigidity or marked reduction in spontaneous movement.
N-methyl-D-aspartate receptor (NMDAR) antibody encephalitis is particularly associated with combinations of dyskinesias, abnormal postures, speech dysfunction, and altered consciousness. These features overlap with other disorders.[3]
Seizures and episodic motor findings
Autoimmune encephalitis may be associated with observed focal motor seizures, behavioral arrest, impaired awareness, generalized convulsions, or status epilepticus.
Leucine-rich glioma-inactivated protein 1 (LGI1) antibody encephalitis can produce faciobrachial dystonic seizures: very brief, often frequent contractions involving the face and arm, sometimes the leg. These episodes may precede overt cognitive impairment.[6]
Clinical observation may not reliably distinguish seizures from dyskinesias or identify non-convulsive seizures. Electroencephalography (EEG) can help resolve this distinction.[4]
Motor, sensory, and reflex findings
Autoimmune encephalitis has no single obligatory pattern of weakness, sensory loss, or tendon-reflex abnormality. Focal deficits, rigidity, or associated peripheral nerve findings may occur depending on the syndrome. Their distribution may also suggest a competing or overlapping neurological disorder.[4]
Coordination and gait
Autoimmune encephalitis with cerebellar involvement may produce ataxia, dysmetria, or an unsteady gait. Gait assessment may be limited by reduced consciousness, agitation, weakness, or abnormal movements.[4]
Examination in Children and Adolescents
Autoimmune encephalitis in children may be associated with reduced engagement, acquired speech impairment, agitation, abnormal movements, seizures, ataxia, or focal weakness. Interpretation requires comparison with age-appropriate abilities and the child's developmental baseline.[7]
Young children may show loss of previously acquired language or functional skills rather than a clearly demonstrable adult-type memory syndrome. Movement abnormalities can be prominent in pediatric NMDAR antibody encephalitis.[7]
Findings Requiring Urgent Assessment
Autoimmune encephalitis with deteriorating consciousness, repeated or prolonged seizures, respiratory compromise, or marked autonomic instability requires urgent assessment. Sedatives, antiseizure medicines, and antipsychotics may alter responsiveness, muscle tone, and movement findings; medication exposure must be considered when interpreting serial examinations.[2][1]
Related Microchapters
References
- ↑ 1.0 1.1 1.2 1.3 1.4 Hahn C, Budhram A, Alikhani K; et al. (2024). "Canadian Consensus Guidelines for the Diagnosis and Treatment of Autoimmune Encephalitis in Adults". Canadian Journal of Neurological Sciences. 51 (6): 734–754. doi:10.1017/cjn.2024.16. PMID 38312020 Check
|pmid=value (help). - ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Michael BD, Huang Y, McKeever S; et al. (2026). "Management of suspected infectious and autoimmune encephalitis in adults – National Guidelines from the United Kingdom Joint Societies". Journal of Infection: 106873. doi:10.1016/j.jinf.2026.106873. PMID 42863638 Check
|pmid=value (help). - ↑ 3.0 3.1 3.2 3.3 3.4 Graus F, Titulaer MJ, Balu R; et al. (2016). "A clinical approach to diagnosis of autoimmune encephalitis". The Lancet Neurology. 15 (4): 391–404. doi:10.1016/S1474-4422(15)00401-9. PMID 26906964.
- ↑ 4.0 4.1 4.2 4.3 4.4 Abboud H, Probasco JC, Irani S; et al. (2021). "Autoimmune encephalitis: proposed best practice recommendations for diagnosis and acute management". Journal of Neurology, Neurosurgery & Psychiatry. 92 (7): 757–768. doi:10.1136/jnnp-2020-325300. PMID 33649022 Check
|pmid=value (help). - ↑ van Sonderen A, Ariño H, Petit-Pedrol M; et al. (2016). "The clinical spectrum of Caspr2 antibody-associated disease". Neurology. 87 (5): 521–528. doi:10.1212/WNL.0000000000002917. PMID 27371488.
- ↑ Thompson J, Bi M, Murchison AG; et al. (2018). "The importance of early immunotherapy in patients with faciobrachial dystonic seizures". Brain. 141 (2): 348–356. doi:10.1093/brain/awx323. PMID 29272336.
- ↑ 7.0 7.1 Cellucci T, Van Mater H, Graus F; et al. (2020). "Clinical approach to the diagnosis of autoimmune encephalitis in the pediatric patient". Neurology: Neuroimmunology & Neuroinflammation. 7 (2): e663. doi:10.1212/NXI.0000000000000663. PMID 31953309.