Description
Brain (head) MRI is the procedure of choice for most brain disorders. It provides clear images of the brainstem and posterior brain, which are difficult to view on a CT scan. It is also useful for the diagnosis of demyelinating disorders (such as multiple sclerosis (MS) that cause destruction of the myelin sheath of the nerve). The evaluation of blood flow and the flow of cerebrospinal fluid (CSF) is possible with this non-invasive procedure.

MRI for headache — Generally, magnetic resonance imaging is the preferred imaging technique for evaluating the brain parenchyma, and CT is preferable for evaluating subarachnoid hemorrhage. CT is faster and more readily available than MRI and is often used in urgent clinical situations. Neurologic imaging is warranted in patients with headache disorders along with abnormal neurologic examination results or predisposing factors for brain pathology. Contrast-enhanced MRI is performed for evaluation of inflammatory, infectious, neoplastic, and demyelinating conditions.

Headache time frames and other characteristics — Generally, acute headaches are present from hours to days, subacute from days to weeks and chronic headaches for more than 3 months. Acute severe headaches are more likely to be pathological (e.g., SAH, cerebral venous thrombosis) than non-acute (e.g., migraine, tension-type). Headaches can also be categorized as new onset or chronic/recurrent. Non-acute new onset headaches do not require imaging unless there is a red flag as delineated above. Incidental findings lead to additional medical procedures and expense that do not improve patient well-being. Primary headache syndromes, such as migraine and tension headaches, are often episodic with persistent or progressive headache not responding to treatment requiring further investigation (e.g., new daily persistent headache). Imaging is indicated in chronic headaches if there is a change in the headache frequency (number of headaches episodes/month), duration of each episode, severity of the headaches or new characteristics, such as changing aura or associated symptoms.^{1,6,215,216,217}

Migraine with aura^6,7,218 — The headache phase of a migraine is preceded and/or accompanied by transient neurological symptoms referred to as aura in at least a third of migraine attacks. The most common aura consists of positive and/or negative visual phenomena, present in up to 99% of the individuals. Somatosensory is the secondary most common type of aura (mostly paresthesia’s in an upper limb and/or hemiface). Language/speech (mainly paraphasia and anomic aphasia) can also be affected. These neurological symptoms typically evolve over a period of minutes and may last up to 20 minutes or more. The gradual evolution of symptoms is thought to reflect spreading of a neurological event across the visual and somatosensory cortices. Characteristically, the aura usually precedes and terminates prior to headache, usually within 60 minutes. In others, it may persist or begin during the headache phase. ICHD-3 definition of the aura of migraine with typical aura consists of visual and/or sensory and/or speech/language symptoms, but no motor, brainstem or retinal symptoms and is characterized by gradual development, duration of each symptom no longer than one hour, a mix of positive and negative features and complete reversibility. Atypical or complex aura includes motor, brainstem, monocular visual disturbances, or ocular cranial nerve involvement (hemiplegic migraine, basilar migraine/brainstem aura, retinal migraine, ophthalmoplegic migraine) and secondary causes need to be excluded. Additional features of an aura that raise concern for an underlying vascular etiology include late age of onset, short duration, evolution of the focal symptoms, negative rather than positive visual phenomenon, and history of vascular risk factors.

Neurological deficits — Examples of abnormal reflexes related to upper motor neuron lesion/central pathology include hyperreflexia, clonus, Hoffman sign and Babinski, snout, palmar grasp, and rooting reflexes.

Visual loss has many possible etiologies, and MRI is only indicated in suspected neurological causes of visual loss based on history and exam. Visual field defects, such as bitemporal hemianopsia, homonymous hemianopsia, or quadranopsia, require imaging as well as does suspected optic nerve pathology. Subjective symptoms such as blurred vision or double vision with no clear correlate on neurological examination requires a comprehensive eye evaluation to exclude more common causes, such as cataracts, refractive errors, retinopathy, glaucoma, or macular degeneration. Transient visual loss with history consistent with TIA but normal exam at time of examination also should be imaged. Positive visual phenomena, such as photopsias or scintillations that march across the visual field, suggest migraine whereas negative phenomenon, such as shaded or blurred, is more characteristic of ischemia.
 
Table 1: Gait and brain imaging^{219,220,221,222,223,224}

Non-neurological causes of gait dysfunction include pain (antalgic), side effects of drugs (analgesic, antihistamines, benzos, psych meds, antihypertensives), visual loss, hearing impairment, orthopedic disorders, rheumatologic disorders, psychogenic, and cardiorespiratory problems (orthostasis).^{220,222,223,224}

MRI and recent stroke or transient ischemic attack — A stroke or central nervous system infarction is defined as “brain, spinal cord, or retinal cell death attributable to ischemia, based on neuropathological, neuroimaging, and/or clinical evidence of permanent injury. … Ischemic stroke specifically refers to central nervous system infarction accompanied by overt symptoms, whereas silent infarction causes no known symptoms.”²²⁵ If imaging or pathology is not available, a clinical stroke is diagnosed by symptoms persisting for more than 24 hours. Ischemic stroke can be further classified by the type and location of ischemia and the presumed etiology of the brain injury. These include large-artery atherosclerotic occlusion (extracranial or intracranial), cardiac embolism, small-vessel disease and less commonly dissection, hypercoagulable states, sickle cell disease and undetermined causes.²²⁶ TIAs in contrast, “are a brief episode of neurological dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction on imaging.”²²⁷ On average, the annual risk of future ischemic stroke after a TIA or initial ischemic stroke is 3% – 4%, with an incidence as high as 11% over the next 7 days and 24% – 29% over the following 5 years. This has significantly decreased in the last half century due to advances in secondary prevention.²²⁸

Therefore, when revascularization therapy is not indicated or available in individuals with an ischemic stroke or TIA, the focus of the work-up is on secondary prevention. This includes noninvasive vascular imaging to identify the underlying etiology, assess immediate complications and risk of future stroke. The majority of stroke evaluations take place in the inpatient setting. Admitting TIA patients is reasonable if they present within 72 hours and have an ABCD(2) score ≥ 3, indicating high risk of early recurrence, or the evaluation cannot be rapidly completed on an outpatient basis.²²⁷ Minimally, both stroke and TIA should have an evaluation for high-risk modifiable factors, such as carotid stenosis atrial fibrillation as the cause of ischemic symptoms.²²⁶ Diagnostic recommendations include neuroimaging evaluation as soon as possible, preferably with magnetic resonance imaging, including DWI; noninvasive imaging of the extracranial vessels should be performed, and noninvasive imaging of intracranial vessels is reasonable.²²⁹
Individuals with a history of stroke and recent work-up with new signs or symptoms indicating progression or complications of the initial CVA should have repeat brain imaging as an initial study. Individuals with remote or silent strokes discovered on imaging should be evaluated for high-risk modifiable risk factors based on the location and type of the presumed etiology of the brain injury.

Non-aneurysmal vascular malformations — Non-aneurysmal vascular malformations can be divided in low flow vascular malformations and high flow vascular malformations. Low flow vascular malformations include dural venous anomalies (DVA), cavernomas, and capillary telangiectasias. High flow vascular malformations include AVM and dural arteriovenous fistulas (dAVF). For low flow malformations, MRI is the study of choice. Limited medical literature is available to support vascular imagining (CTA or MRA). CTA plays a limited role in the assessment of cavernoma but may be used to demonstrate a DVA. MRA is not usually helpful in the assessment of cavernoma, capillary telangiectasia, and DVA. Vascular imaging is indicated in high flow vascular malformations.^230,231,232

MRI and central venous thrombosis — An MR venogram is indicated for the definite evaluation of a central venous thrombosis/dural sinus thrombosis. The most frequent presentations are isolated headache, intracranial hypertension syndrome (headache, nausea/vomiting, transient visual obscurations, pulsatile tinnitus, CN VI palsy, papilledema),²³³ seizures, focal neurological deficits, and encephalopathy. Risk factors are hypercoagulable states inducing genetic prothrombotic conditions, antiphospholipid syndrome and other acquired prothrombotic diseases (such as cancer), oral contraceptives, pregnancy, puerperium (6-weeks postpartum), infections, and trauma. COVID-19 infection is associated with hypercoagulability, a thromboinflammatory response, and an increased incidence of venous thromboembolic events (VTE).^234,235 Since venous thrombosis can cause SAH, infarctions, and hemorrhage, parenchymal imaging with MRI/CT is also appropriate.^27,236,237
 
Galactorrhea and MRI — Isolated galactorrhea without elevated prolactin (normoprolactinemic) is usually due to breast pathology, i.e., breast feeding, trauma, ill-fitting undergarments. Consider mammogram, breast ultrasound, and serial dilution of the individual’s prolactin sample to correct for possible hook effect.^238,239

Chart 1: Causes of Hyperprolactinemia²⁴⁰

Table 2: MRI and Staging Screening in Non-CNS Cancers^53,54,56,58

Surveillance for trilateral heritable retinoblastoma (Pineoblastoma surveillance)
Brain MRI at the time of retinoblastoma diagnosis; some centers recommend a brain MRI every 6 months until 5 years old^241,242

MRI and Neurocutaneous Syndromes

• In NF-1, clinical evaluation appears to be more useful to detect complications than is screening imaging in asymptomatic individuals. Imaging is indicated in evaluation of suspected tumors based on clinical evaluation and for follow-up of known intracranial tumors.²⁴³
• Conversely in NF-2, routine MR imaging screening is always indicated, given the high prevalence of CNS tumors, especially vestibular schwannomas. In individuals with NF-2, routine screening brain/IAC imaging is indicated annually starting from age 10 if asymptomatic or earlier with clinical signs/symptoms. Most individuals with NF2 eventually develop a spinal tumor, most commonly schwannomas, but meningioma and ependymomas are also seen. Spinal imaging at baseline and every 2 to 3 years is also advised with more frequent imaging, if warranted, based on sites of tumor involvement.⁶⁸
• In individuals with Tuberous Sclerosis, Brain MRI should be obtained every 1-3 years up until age 25 for surveillance for CNS abnormalities.⁶⁶
• In Von Hippel Lindau Syndrome, imaging of the brain and spinal cord for hemangioblastomas is recommended every 2 years.⁶⁵
• In Sturge Weber Syndrome, Brain MRI can rule out intracranial involvement only after age 1 and is recommended in individuals < 1 year only if symptomatic.⁶⁹

Multiple sclerosis^95,244,245 — The diagnosis of MS requires demonstration of lesions in the CNS disseminated in time and space and the absence of fever, infection, or other more likely etiologies. An expanding amount of available disease-modifying treatments are effective in slowing down disease progression, especially in the early stages. These treatments can have serious side effects and can be costly; therefore, the accurate and expeditious diagnosis of MS is critical.

The diagnosis of MS can be made on clinical presentation alone with 2 clinical attacks and objective clinical evidence of more than 2 lesions. Attacks may be individual-reported or objectively observed and must last for a minimum of 24 hours and be 30 days apart. However, corroborating magnetic resonance imaging (MRI) is the diagnostic standard and is used, as well, to rule out other disorders. Additionally, MRI findings can replace certain clinical criteria in a substantial number of individuals. In the revised McDonald Criteria, MRI findings can be used to establish dissemination in both time and space.

 
In the presence of a clear, clinically isolated syndrome such as optic neuritis, transverse myelitis, or brain stem syndrome, brain MRI is the next diagnostic step. MS can also have variable and often subjective symptoms that come and go (see Table 3). If there are recurrent episodes of variable neurological signs or symptoms not attributable to another cause with clinical concern for MS, imaging is warranted as well.

MRI and neuromyelitis optica spectrum disorders (NMOSD)²⁰³ — NMOSD are inflammatory disorders of the central nervous system characterized by severe, immune-mediated demyelination and axonal damage predominantly affecting the optic nerves and spinal cord, but also the brain and brainstem.

NMOSD can be distinguished from multiple sclerosis and other inflammatory disorders by the presence of the aquaporin-4 (AQP4) antibody. Features of NMOSD include attacks of bilateral or sequential optic neuritis acute transverse myelitis and the area postrema syndrome (with intractable hiccups or nausea and vomiting). The evaluation of suspected NMOSD entails brain and spinal cord neuroimaging. In contrast to MS (in which spinal cord involvement tends to be incomplete and asymmetric), NMOSD have a longer extent of spinal cord demyelination generally involving three or more vertebral segments.

Temporal arteritis — Giant cell arteritis (GCA) is an inflammatory disorder that should be considered in individuals over the age of 50 with the following signs or symptoms: new headaches, acute onset of visual disturbances (especially transient monocular visual loss), jaw claudication, constitutional symptoms, tenderness over the temporal artery, and elevated ESR and/or CRP. A diagnosis of polymyalgia rheumatica (PMR) is highly associated. Large vessel GCA denotes involvement of the aorta and its first-order branches, especially the subclavian arteries, and is common. Extra- and intracranial cerebral vasculitis can also be seen but is rarer, and strokes are related to vasculitis of extracranial cerebral arteries causing vertebral or internal carotid arteries stenosis. Gold standard for diagnosis of GCA is temporal artery biopsy. Color Doppler ultrasound (CDUS) can be used as a surrogate for temporal artery biopsy in some cases. High-resolution magnetic resonance imaging (MRI) can visualize the temporal arteries when used with contrast. The presence of clinical manifestations unusual in GCA should prompt consideration of alternative diagnoses. Examples of such include adenopathy, pulmonary infiltrates, digital cyanosis, ulceration or gangrene, mononeuritis multiplex, stroke in the distribution of the middle cerebral artery, glomerulitis, and/or rapidly rising creatinine.^{103,104,105,106,107,246}

MMSE — The Mini Mental State Examination (MMSE) is a tool that can be used to assess mental status systematically and thoroughly. It is an 11-question measure that tests five areas of cognitive function: orientation, registration, attention and calculation, recall, and language. The MMSE has been the most commonly used measure of cognitive function in dementia research, but researchers have recognized that it is relatively insensitive and variable in mildly impaired individuals. The maximum score is 30. A score of 23 or lower is indicative of cognitive impairment. The MMSE takes only 5 – 10 minutes to administer and is, therefore, practical to use repeatedly and routinely.

MoCA — The Montreal Cognitive Assessment (MoCA) was designed as a rapid screening instrument for mild cognitive dysfunction. It assesses different cognitive domains: attention and concentration, executive functions, memory, language, visuoconstructional skills, conceptual thinking, calculations, and orientation. MoCA differs from the MMSE mainly by including tests of executive function and abstraction, and by putting less weight on orientation to time and place. Ten of the MMSE's 30 points are scored solely on the time-place orientation test, whereas the MoCA assigns it a maximum of six points. The MoCA also puts more weight on recall and attention-calculation performance, while de- emphasizing language skill. Time to administer the MoCA is approximately 10 minutes. The total possible score is 30 points; a score of 26 or above is considered normal.

MRI and movement disorders — Atypical parkinsonian syndromes include progressive supranuclear palsy (PSP), multiple system atrophy (MSA), corticobasal degeneration (CBD), and dementia with Lewy bodies.

Anosmia — Nonstructural causes of anosmia include post-viral symptoms, medications (Amitriptyline, Enalapril, Nifedipine, Propranolol, Penicillamine, Sumatriptan, Cisplatin, Trifluoperazine, Propylthiouracil). These should be considered prior to advanced imaging to look for a structural cause.

Anosmia and dysgeusia have been reported as common early symptoms in individuals with COVID-19, occurring in greater than 80 percent of individuals. For isolated anosmia, imaging is typically not needed once the diagnosis of COVID has been made given the high association. As such, COVID testing should be done prior to imaging.^247,248,249

MRI orbits, face, and neck MRI rather than MRI brain is the mainstay for directly imaging the olfactory apparatus and sinonasal or anterior cranial fossa tumors that may impair or directly involve the olfactory apparatus.

Trigeminal neuralgia (TN) — According to the International Headache Society, TN is defined as “a disorder characterized by recurrent unilateral brief electric shock-like pain, abrupt in onset and termination, limited to the distribution of one or more divisions of the trigeminal nerve and triggered by innocuous stimuli.”⁶ Atypical features include bilateral, hearing loss, dizziness/vertigo, visual changes, sensory loss, numbness, pain > 2 min, pain outside trigeminal nerve distribution and progression.^140,214

Occipital neuralgia — According to the International Headache Society, occipital neuralgia is defined “Unilateral or bilateral paroxysmal, shooting or stabbing pain in the posterior part of the scalp, in the distribution(s) of the greater, lesser and/or third occipital nerves, sometimes accompanied by diminished sensation or dysesthesia in the affected area and commonly associated with tenderness over the involved nerve(s). Pain is eased temporarily by local anesthetic block of the affected nerve(s). Occipital neuralgia must be distinguished from occipital referral of pain arising from the atlantoaxial or upper zygapophyseal joints or from tender trigger points in neck muscles or their insertions.”⁶

MRI for macrocephaly — Consider ultrasound in infants with macrocephaly and a normal neurological examination, no evidence of increased ICP and an open anterior fontanelle. If head US is normal, the infant should be monitored closely.²⁵⁰ The anterior fontanelle generally closes between 10 and 24 months of age, with 3% closing between 5 – 9 months and 11% after 24 months.²⁵¹

MRI and normal pressure hydrocephalus (NPH) — Although diagnosis can be made based on CT findings alone, MRI is more accurate for disclosing associated pathologies (such as cerebrovascular disease), excluding other potential etiologies and for detecting NPH typical signs of prognostic value. A CT scan can exclude NPH and is appropriate for screening purposes and in individuals who cannot undergo MRI.¹⁵³

MRI and vertigo — The most common causes of vertigo seen are benign paroxysmal positional vertigo (BPPV), vestibular neuronitis (VN) and Ménière’s disease. These peripheral causes of vertigo are benign, and treatment involves reassurance and management of symptoms. Central causes of vertigo, such as cerebrovascular accidents (CVAs), tumors and multiple sclerosis (MS), need to be considered if the individual presents with associated neurological symptoms, such as weakness, diplopia, sensory changes, ataxia, or confusion. Magnetic resonance imaging is appropriate in the evaluation of individuals with vertigo who have neurologic signs and symptoms, progressive unilateral hearing loss or risk factors for cerebrovascular disease. MRI is more appropriate than CT for diagnosing vertigo due to its superiority in visualizing the posterior portion of the brain, where most central nervous system disease that causes vertigo is found. A full neurologic and otologic evaluation including provocative maneuvers, vestibular function testing and audiogram can help evaluate vertigo of unclear etiology and differentiate between central and peripheral vertigo.

MRI and developmental delay — Significant developmental delay is defined as significant delay (more than two standard deviations below the mean) in one or more developmental domains: gross/fine motor, speech/language, cognition, social/personal, and activities of daily living. Isolated delay in social/language development is characteristic of autism spectrum disorders or hearing loss. Isolated delay in motor development is characteristic of cerebral palsy (a static encephalopathy) or myopathy.
Global developmental delay (GDD) is a subset of developmental delay defined as significant delay (by at least 2 SD’s) in two or more developmental categories. Note that the term “GDD” is usually reserved for children < 5 years old, whereas in older children > 5 years, disability is quantifiable with IQ testing. The yield of magnetic resonance imaging is low in children with autism spectrum disorder and no other neurologic findings; therefore, MRI is not recommended as a part of routine evaluation.²⁵²

Low-risk brief resolved unexplained event (BRUE) formerly apparent life-threatening event (ALTE) requires all the following:

• Age > 60 days
• Gestational age ≥ 32 weeks or older and corrected gestational age > 45 weeks
• First brief event
• Event lasting < 1 minute
• No CPR required by the trained medical provider
• No concerning historical features or physical examination findings.

Combination MRI/MRA of the brain — This is one of the most misused combination studies and other than what is indicated above these examinations should be ordered in sequence, not together. Vascular abnormalities can be visualized on the brain MRI.

Individuals presenting with a new migraine with aura (especially an atypical or complex aura) can mimic a transient ischemic attack or an acute stroke. If there is a new neurologic deficit, imaging should be guided by concern for cerebrovascular disease, not that the individual has a headache.^11,197
 
Leptomeningeal carcinomatosis^{253,254,255,256} — Leptomeningeal metastasis is an uncommon and typically late complication of cancer with poor prognosis and limited treatment options. Diagnosis is often challenging with nonspecific presenting symptoms ranging from headache and confusion to focal neurologic deficits such as cranial nerve palsies. Standard diagnostic evaluation involves a neurologic examination, MRI of the brain and spine with gadolinium, and cytologic evaluation of the cerebral spinal fluid (CSF). Hematologic malignancies (leukemia and lymphoma), primary brain tumors as well as solid malignancies can spread to the leptomeninges. The most common solid tumors giving rise to LM are breast cancer (12% – 35%), small and non-small cell lung cancer (10% – 26 %), melanoma (5% – 25%), gastrointestinal malignancies (4% – 14%), and cancers of unknown primary (1% – 7%).

Drop metastases — Drop metastases are intradural extramedullary spinal metastases that arise from intracranial lesions. Common examples of intracranial neoplasms that result in drop metastases include pineal tumors, ependymomas, medulloblastomas, germinomas, primitive neuroectodermal tumors (PNET), glioblastomas multiform, anaplastic astrocytomas, oligodendrogliomas and less commonly choroid plexus neoplasms and teratomas.²⁵⁷

GENERAL INFORMATION

It is an expectation that all patients receive care/services from a licensed clinician. All appropriate supporting documentation, including recent pertinent office visit notes, laboratory data, and results of any special testing must be provided. If applicable: All prior relevant imaging results and the reason that alternative imaging cannot be performed must be included in the documentation submitted.

Where a specific clinical indication is not directly addressed in this guideline, medical necessity determination will be made based on widely accepted standard of care criteria. These criteria are supported by evidence-based or peer-reviewed sources such as medical literature, societal guidelines and state/national recommendations.
 

Policy 
INDICATIONS FOR BRAIN MRI
Brain MR/MRA are not approvable simultaneously unless they meet the criteria described below in the Indications for Brain MR/Brain MRA combination studies section. If there is a combination request* for an overlapping body part, either requested at the same time or sequentially (within the past 3 months) the results of the prior study should be:

• • • If atypical presentation (bilateral, absence of pain, optic nerve hemorrhages, severe visual impairment, lack of response to steroids, poor recovery or recurrence)^209,210
    • If needed to confirm optic neuritis and rule out compressive lesions
  • Known or suspected neuromyelitis optica spectrum disorder with severe, recurrent, or bilateral optic neuritis²⁰³
  • Suspected retinoblastoma^211,212
• Brain MRI/FACE/SINUS/NECK MRI
  • Granulomatosis with polyangiitis (Wegener’s granulomatosis) disease²¹³
  • Trigeminal neuralgia or neuropathy with an atypical presentation (for evaluation of the extracranial nerve course) ^140,214 See Background.
  • Bell’s Palsy/hemifacial spasm for evaluation of the extracranial nerve course -if atypical signs, slow resolution beyond three weeks, no improvement at four months, or facial twitching/spasms prior to onset¹³⁸
  • Objective cranial nerve palsy (CN IX-XII) (for evaluation of the extracranial nerve course)^140,141

References 

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ADDITIONAL RESOURCES

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Procedure and diagnosis codes on Medical Policy documents are included only as a general reference tool for each policy. They may not be all-inclusive. 

This medical policy was developed through consideration of peer-reviewed medical literature generally recognized by the relevant medical community, U.S. FDA approval status, nationally accepted standards of medical practice and accepted standards of medical practice in this community, Blue Cross Blue Shield Association technology assessment program (TEC) and other nonaffiliated technology evaluation centers, reference to federal regulations, other plan medical policies, and accredited national guidelines.

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