Measles: neurologic complications …

Infectious Disorders

Updated 05.29.2024
Released 05.26.2015
Expires For CME 05.29.2027

Measles: neurologic complications

Authors: Elena Grebenciucova MD, Karen L Roos MD FAAN

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Editor: Christina M Marra MD

Measles: neurologic complications

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Introduction

This article includes discussion of central nervous system syndromes associated with measles infection, primary measles encephalitis, acute post-infectious measles encephalomyelitis, measles inclusion body encephalitis, and subacute sclerosing panencephalitis (SSPE). The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Measles, or rubella, is caused by a single stranded negative-sense RNA virus that belongs to the Morbillivirus genus of the Paramyxoviridae family (11) and is considered to be one of the most contagious infections known. Measles is typically spread via respiratory aerosol. Even in developed countries, mortality remains close to 3 in 1000 of those infected (44). Despite worldwide efforts of measles eradication and the availability of a preventive vaccine since the 1960s, outbreaks remain frequent. Measles has reemerged as a major public health problem in the last decade. Between January and August 2019, there have been over 1000 cases of measles confirmed in the United States alone. This is the highest number reported since measles were considered eliminated in 2000 (07).

Failure to vaccinate is the most common reason for the current increase in measles (07). Travel to countries where vaccination programs are lacking, waning immunity, and the lack of antibody production in 2% to 10% of the patients vaccinated also contribute to the reemergence observed in the past decade.

Key points

	• Neurologic syndromes associated with measles include measles inclusion body encephalitis, acute post-infectious measles encephalomyelitis, primary measles encephalitis, and subacute sclerosing panencephalitis.
	• Neurologic sequelae of measles are severe and, depending on the syndrome, may carry a substantial risk of disability and even death.
	• Measles vaccination is highly effective in preventing primary infection. It does not cause autism.

Historical note and terminology

Some of the first descriptions of measles infection are believed to belong to Chinese alchemist and philosopher, Kong Hu, circa 300 C.E. Several centuries later, in 910, an Iranian physician, Abu Bakr Mohammad Ibn Zakariya al-Razi, known simply as Rhazes, published a treatise on the diagnostic differentiation of measles and chickenpox.

When, therefore, you see these symptoms, or some of the worst of them (such as pain of the back, and the terrors of sleep, with the continued fever) then you may be assured that the eruption of one or the other of these diseases in the patient is nigh at hand; except that there is not in the measles so much pain of the back as in smallpox; nor in the smallpox so much anxiety and nausea as in measles, unless the smallpox be of a bad sort; and this shows that the measles came from a very bilious blood (24).

The first measles inoculation attempts in the Western world are ascribed to Francis Home, a Scottish physician, who, in 1757, demonstrated that measles was caused by an infectious agent by inoculating several groups of children with blood and nasal discharge from patients with measles (13).

The measles virus was first cultivated in kidney cell tissue by Thomas Peebles, a World War II bomber pilot turned pediatrician, who at that time was working with Enders, one of the most renowned virologists of the 20th century who invented the technique of viral tissue cultures, culminating in the creation of the polio vaccine and subsequently many others (14). Peebles isolated measles from an 11-year-old boy and used that strain to make the very first measles vaccine. The vaccine was approved in the United States in 1963 (02).

Clinical manifestations

Presentation and course

In the central nervous system, measles virus infection can manifest itself as 4 distinct syndromes: primary measles encephalitis, acute post-measles encephalomyelitis, measles inclusion body encephalitis, and perhaps the best known to the reader, subacute sclerosing panencephalitis.

Patients with primary measles encephalitis present with fever, headache, alteration of consciousness, motor deficits, and seizures. In this syndrome, the virus invades and replicates in the brain cells. Subsequent chemokine induction and lymphocytic infiltration may result in significant brain edema, leading to the development of increased intracranial pressure (42). This syndrome typically develops during the exanthema stage of the infection (Fisher et al 2015), although cases preceding the rash have rarely been described (31). Detection of measles virus RNA in the CSF can help establish the diagnosis. The virus can also be isolated from the brain cell cultures (08).

Acute postinfectious measles encephalomyelitis is the most frequent central nervous system complication of measles infection (40) and typically occurs closer toward the resolution phase of the infection or days to months after the infection has cleared. Acute post-measles encephalomyelitis may also rarely occur as a result of vaccination (1 to 2 cases per million) (15; Tenembaum et all 2007).

Unlike primary measles encephalitis, acute post-measles encephalomyelitis is immune-mediated and does not involve invasion of the brain parenchyma by the virus. Symptoms of acute post-measles encephalomyelitis arise secondary to diffuse demyelination. Patients present with altered mental status, motor or sensory deficits, or ataxia. Those with significant spinal cord involvement may have back pain as well as bowel and bladder dysfunction (38). In the very rare instances when acute post-measles encephalomyelitis presents after a measles vaccination, its course is typically less aggressive (09).

Postinfectious measles encephalomyelitis may relapse in one third of patients (35). Because the syndrome is immune mediated, viral RNA typically cannot be isolated from the CSF (20; 27). Magnetic resonance imaging can be used to demonstrate disseminated white matter lesions in the brain and spinal cord (09; 23).

Measles inclusion body encephalitis, also known as immunosuppressive measles encephalitis, subacute measles encephalitis, or acute measles encephalitis of the delayed type, is a syndrome that typically affects immunocompromised children within 1 year of the primary measles infection. This syndrome occurs due to persistent measles infection in the CNS. Cases have been described in association with HIV, autoimmune disorders, and solid organ and stem cell transplantation.

Patients typically present with mental status changes, motor abnormalities, or seizures. Dysarthria and visual disturbances, including cortical blindness, have rarely been described as well (39). Less often, patients present with fever, nausea, vomiting, and emotional lability. In some instances, hypertension and other symptoms of autonomic instability may be seen. Seizures are often refractory to multiple antiepileptic medications (39). Course of the disease is that of progressive neurologic dysfunction over days to weeks, frequently resulting in coma and death (05; 37; 28).

It must be noted that some cases of measles inclusion body encephalitis have been reported in children with no known primary measles infection (28). This is likely due to the fact that the classical morbilliform rash seen in primary measles infection is a result of T-cell-mediated hypersensitivity reaction to the virus, whereas in the immunompromised patients, the typical viral exanthem may be nearly absent, making the correct diagnosis difficult.

Subacute sclerosing panencephalitis predominantly occurs in patients who acquired primary measles infection before the age of 2 years (46). Average delay between primary measles infection and subacute sclerosing panencephalitis is 6 to 15 years (Buchanan and Bonthius 2012). Clinical manifestations are insidious and involve cognitive and behavioral changes in the first stage of the syndrome. Children may present with deterioration in their school performance, whereas adults may develop difficulties at work. Ocular involvement is common and occurs in nearly 50% of cases. Patients present with necrotizing retinitis and in some cases with optic neuritis. Ocular manifestations may precede the onset of symptoms by several years (01). In the second stage of subacute sclerosing panencephalitis, patients develop myoclonus, abnormal movements and postures, and ataxia as well as seizures. Progression into the third stage of the disease is manifested by progressive rigidity and akinetic mutism, culminating in stage 4, which is coma (36; 30). A case of subacute sclerosing panencephalitis, presenting with myoclonic astatic epilepsy, has been described (32).

Subacute sclerosing panencephalitis: periodic myoclonus

This 16-year-old boy had a 5-month history of mental deterioration and generalized periodic myoclonus. EEG revealed generalized periodic discharges, and CSF examination revealed raised anti-measles antibody titer. (Contributed by ...
Subacute sclerosing panencephalitis: subtle myoclonus (1)

This 17-year-old girl with deceasing scholastic performance and electroencephalography showing periodic discharges demonstrates subtle myoclonus. This girl has no apparent periodic myoclonus. (Contributed by Dr. Ravindra Kumar Gar...
Subacute sclerosing panencephalitis: subtle myoclonus (2)

This 13-year-old girl presented with deceased scholastic performance and recurrent falls. This video demonstrates near fall as a manifestation of subtle myoclonus. (Contributed by Dr. Ravindra Kumar Garg.)

Prognosis and complications

Primary measles encephalitis carries 10% to 15% mortality, with about 25% of surviving patients developing permanent neurologic sequelae, such as seizures or cognitive deficits (Buchanan and Bonthius 2012).

Prognosis of patients with acute postinfectious measles encephalomyelitis is overall better than of those with primary measles encephalitis. Estimated mortality is 5% in children and 25% in adults. Some patients may fully recover, whereas others may be left with permanent neurologic sequelae.

A 3-year follow-up study of patients with acute postinfectious measles encephalomyelitis suggested that some children, despite appearing fully recovered, may go on to have long-term behavioral or cognitive deficits (49).

Relapses can be seen in up to one third of patients (35).

Measles inclusion body encephalitis is associated with high mortality, which is estimated at 75% (47), with death ensuing within several weeks of the first symptoms. Treatment is mainly supportive and focuses on cessation of immunosuppressive agents and seizure control. No effective treatment currently exists. Antiviral agents, such as intravenous ribavirin, have been attempted in a few cases, but their efficacy has been limited (39; 17).

Infectious Diseases Society of America guidelines on the treatment of encephalitis state that in measles encephalitis, empiric treatment with ribavirin can be considered (50).

Subacute sclerosing panencephalitis overall has poor prognosis. Most patients survive for only 1 to 3 years after the onset of symptoms. With good supportive measures, some patients have been known to experience remissions lasting weeks to years. A clinical course ranging from 10 to 15 years has been reported (12).

Clinical vignette

An internationally adopted 13-year-old boy presented to his primary care provider with progressive difficulty with his school work over the past month as well as gait ataxia, poor vision in the left eye, and left-sided hemiparesis. The patient’s MRI revealed multifocal hyperintensities. He was initially diagnosed with acute disseminated encephalomyelitis, and high-dose intravenous steroids were initiated. Subsequently, CSF showed a high titer of anti-measles IgG antibodies. EEG was pathognomonic for subacute sclerosing panencephalitis showing Rademecker complexes (generalized periodic discharges). Patient went on to develop myoclonic jerks and within 3 weeks progressed to coma and died. Biopsy of his brain was consistent with subacute sclerosing panencephalitis. Later obtained detailed history revealed an episode of rash, followed by a fever, around the age of 2 years. History of vaccinations was known.

Biological basis

Etiology and pathogenesis

Primary measles encephalitis is caused by the measles virus directly invading the cells of the central nervous system (neurons, oligodendroglia, and astrocytes). The mechanism of this is unclear as nerve cells do not have the CD150 receptor the virus uses peripherally (45). Because a specific receptor for the viral entry into the CNS has not been discovered, it has been suggested that the virus may gain entry to the central nervous system either via endothelial cells or infected monocytes (48).

Unlike its predecessor, acute postinfectious measles encephalomyelitis does not involve direct invasion of the brain cells by the measles virus and, instead, is immune-mediated. Molecular mimicry results in damage to the myelin basic protein and causes diffuse demyelination (18).

Measles inclusion body encephalitis occurs in immunocompromised patients and is thought to be the consequence of their inability to clear the infection. The virus is readily detectable in neurons, oligodendroglia, and astrocytes. Neuropathology shows glial cell proliferation with areas of focal necrosis and perivascular inflammation. Electron microscopy of tissue reveals intracytoplasmic and intranuclear inclusion bodies, consistent with paramyxovirus nucleocapsids (39).

Subacute sclerosing panencephalitis is thought to occur due to viral persistence, and with time, mutation after the primary infection (typically before the age of 2 years) that could not be successfully cleared by the immune system (19).

The fact that children who become infected with measles virus before age 1 are at highest risk for developing subacute sclerosing panencephalitis suggests that the immaturity of the immune system during primary infection is at least in part responsible for the pathogenesis of this disease (21). Analysis of the viral RNA from the infected cells confirms the same lineage as the virus that caused primary measles infection, but with changes in the M, F, and H proteins (51; Mawrin et all 2002).

Nuclear and cytoplasmic viral inclusion bodies can be detected in both neurons and oligodendrocytes. Grey matter is typically affected more profoundly than the white matter. Extensive mononuclear inflammation can be detected in the parenchyma (10).

Gradual nature of spread occurs over years (as can be suggested by serial MRIs), and eventually clinical manifestations become evident (34).

Prevention

The Advisory Committee on Immunization Practices (ACIP) recommends vaccination against measles at the age of 12 to 15 months, followed by a second dose not earlier than 28 days after the first dose (typically around the ages of 4 to 6, preceding school/kindergarten entry).

Postexposure prophylaxis is indicated in people without known acquired immunity to measles. Within 72 hours of exposure, patients should receive the measles vaccine, or alternatively, immunoglobulin infusion within 6 days of exposure. These 2 strategies may prevent, attenuate, or significantly alter the course of the symptomatic infection.

The CDC recommends vaccinating infants under 12 months of age during an epidemic or when many cases in infants below 12 months of age are reported in the community. Those who were vaccinated prior to the age of 12 months need to be revaccinated between 12 and 15 months of age and again at 4 to 6 years of age.

Life-threatening adverse events related to the MMR vaccine are exceedingly rare and have been associated with rare cases of inborn errors in type I and/or type III interferon pathways (mutations in STAT1, STAT2, and IFNAR2) (26).

If exposed to measles virus, people who are immunocompromised should receive measles immunoglobulin infusion regardless of their vaccination status, as they may not be able to mount an immune response of necessary magnitude and are at increased risk for complications and mortality.

Pregnant women represent another high-risk group for complications, both personal and to the unborn fetus. Pregnant women who have not been previously vaccinated should receive immunoglobulin if exposure occurs. MMR is a live vaccine and is contraindicated in pregnancy.

Diagnostic workup

The choice of diagnostic workup should be guided by clinical suspicion of a specific measles-associated neurologic syndrome.

Neurologic symptoms associated with the primary measles encephalitis typically develop within 7 days of the systemic infectious prodrome. CSF is usually abnormal with lymphocytic pleocytosis and elevated protein concentration (39). Due to the diffuse inflammatory process, brain edema may ensue, and opening pressure may be significantly elevated. Diagnosis of primary measles encephalitis can be further supported when measles virus RNA is detected in the CSF by polymerase chain reaction (33). CNS symptomatic involvement in a patient with symptoms of measles or with peripheral anti-measles IgM antibodies should raise a strong suspicion of primary measles encephalitis, and CSF diagnostic tests should be performed.

Acute post-measles encephalitis by definition precludes detection of measles virus RNA in the CSF. This syndrome is post-infectious and immune-mediated in nature (27). MRI and CSF are helpful in establishing the diagnosis. Lymphocytic pleocytosis and elevated protein concentration may be present in the CSF. IgG index in the CSF is usually not elevated. MRI shows disseminated white matter lesions in the brain or spine (41; 09).

In measles inclusion body encephalitis, CSF may initially be normal, although mild pleocytosis and an elevated protein concentration may be present (48; 39). With progression of the disease, CSF anti-measles antibody titers rise. In fact, over the course of the disease, in 50% of cases, a 4-fold increase in the CSF antibody titers is expected (39).

Diagnosis is confirmed via biopsy of the brain with detection of viral RNA by PCR or viral antigen via immunohistochemistry specific for measles matrix and hemagglutinin proteins (48). The virus can also be isolated from cerebral tissue and by polymerase chain reaction from CSF (Buchanan and Bonthius 2012; 25).

MRI of the brain is usually normal but occasionally may reveal atrophy, ventriculomegaly, or edema (48).

EEG may be abnormal and may reveal focal or multifocal epileptiform discharges. Focal motor seizures or even epilepsia partialis continua may occur.

Neuropathologic examination may show glial proliferation and areas of necrosis and perivascular inflammation. Electron microscopy may detect intracytoplasmic or intranuclear inclusions consisting of measles virus nucleocapsids (39).

Diagnosis of subacute sclerosing panencephalitis is suspected by the clinical presentation, as discussed in the section above. Titers of anti-measles antibodies in the CSF are typically very high. MRI scans can be used to monitor progression of the disease. Initially, lesions are present in the gray matter, but as the disease progresses, these appear in the periventricular white matter and progressively affect deeper structures as well as brainstem (Fisher et al 2015).

EEG findings may consist of periodic slow-wave complexes, every 4 to 10 seconds, accompanied by myoclonic spasms (04).

Media

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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Authors

Elena Grebenciucova MD

Dr. Grebenciucova of Northwestern University has no relevant financial relationships to disclose.
See Profile
Karen L Roos MD FAAN

Dr. Roos of Indiana University School of Medicine has no relevant financial relationships to disclose.
See Profile

Editor

Christina M Marra MD

Dr. Marra of the University of Washington School of Medicine has no relevant financial relationships to disclose.
See Profile

Patient Profile

Age range of presentation: 0-01 month

01-23 months

02-05 years

06-12 years

13-18 years

19-44 years

45-64 years

65+ years
Sex preponderance: Female = male
Heredity: None
Population groups selectively affected: None
Occupation groups selectively affected: None

ICD & OMIM codes

ICD-9: Postmeasles encephalitis: 055.0

Postmeasles otitis media: 055.2

Measles with other specified complications: 055.7

Subacute sclerosing panencephalitis: A81.1
ICD-10: Measles complicated by encephalitis: B05.0

Encephalitis, myelitis and encephalomyelitis in viral diseases classified elsewhere: G05.1

Measles complicated by otitis media: B05.3

Otitis media in viral diseases classified elsewhere: H67.1

Measles with other complications: B05.8

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Measles: neurologic complications

Associated Disorders

Encephalomyelitis
Bowel and bladder dysfunction
Brain edema
Increased intracranial pressure
Inclusion body encephalitis
- Necrotizing retinitis
- Optic neuritis
- Seizures
- Subacute sclerosing panencephalitis

Differential Diagnosis

autoimmune encephalomyelitis
neoplastic encephalomyelitis
paraneoplastic encephalomyelitis
postinfectious encephalomyelitis
systemic lupus erythematosus
- sarcoidosis
- multiple sclerosis
- neuromyelitis optica
- Behcet disease

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Clinical Categories

Infectious Disorders

Measles: neurologic complications …

Measles: neurologic complications