MRI Brain (Includes Internal Auditory Canal) - CAM 744HB

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 aura6,7,218 — 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 imaging219,220,221,222,223,224



Work up/Imaging


Spastic unilateral, circumduction

Brain and/or cervical spine imaging

based on associated symptoms


Spastic bilateral, circumduction

Brain, cervical and thoracic spine



Wide based, stiff, unsteady

Cervical and/or thoracic spine MRI

based on associated symptoms


Broad based, clumsy, staggering, lack of coordination, usually also

with limb ataxia

Brain imaging


Magnetic, shuffling, difficulty


Brain imaging


Stooped, small steps, rigid,

turning en bloc, decreased arm swing

Brain imaging


Irregular, jerky, involuntary movements

Medication review, consider brain

imaging as per movement disorder brain MR guidelines

Sensory ataxic

Cautious, stomping, worsening without visual input (i.e., +


EMG, blood work, consider spinal (cervical or thoracic cord imaging)

imaging based on EMG


Steppage, dragging of toes

EMG, if there is foot drop, Lumbar spine MRI

Pelvis MR appropriate evidence of plexopathy


Insecure, veer to one side, worse

when eyes closed, vertigo

Consider brain/IAC MRI as per GL

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




  1. Coitus
  2. Exercise
  3. Lactation
  4. Pregnancy
  5. Sleep
  6. Stress













  1. Hypothalamic-pituitary stalk damage
    1. Granulomas
    2. Infiltrations
    3. Irradiation
    4. Rathke’s cyst
    5. Trauma: pituitary stalk section, suprasellar surgery
    6. Tumors: craniopharyngioma, germinoma, hypothalamic metastases, meningioma, suprasellar pituitary mass extension
  2. Pituitary
    1. Acromegaly
    2. Idiopathic
    3. Lymphocytic hypophysitis or parasellar mass
    4. Macroadenoma (compressive)
    5. Macroprolactinemia
    6. Plurihormonal adenoma
    7. Prolactinoma
    8. Surgery
    9. Trauma
  3. Systematic Disorders
    1. Chest — neurogenic chest wall trauma, surgery, herpes zoster
    2. Chronic renal failure
    3. Cirrhosis
    4. Cranial radiation
    5. Epileptic seizures
    6. Polycystic ovarian disease
    7. Pseudocyesis





  1. Anesthetics
  2. Anticonvulsant
  3. Antihistamines (H2)
  4. Antihypertensives
  5. Cholinergic agonist
  6. Drug-induced hypersecretion
  7. Catecholamine depletory
  8. Dopamine receptor blockers


  1. Dopamine synthesis inhibitor
  2. Estrogens: oral contraceptives, oral contraceptive withdrawal
  3. Neuroleptics/antipsychotics

Table 2: MRI and Staging Screening in Non-CNS Cancers53,54,56,58



Cutaneous melanoma

Stage IIIC or higher, default staging screening

≥ stage IIIC, surveillance with periodic brain MRI up to 3 years even if asymptomatic without prior brain mets; and if prior brain mets, surveillance every 3 – 6 months up to 3 years

Testicular cancer-Seminoma

If high risk, such as beta HCG > 5000IU/L, or multiple lung or visceral mets, choriocarcinoma, neurological symptoms, or

AFP > 10,000ng/ml

Merkel cell carcinoma

Default staging screening, but especially for high risk (≥ stage

IIIb, immunosuppression)

Lung cancer

Default staging screening

brain MRI also for surveillance in small cell every 3 months for 2 years if they have had no prophylactic cranial radiation

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 old241,242

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 sclerosis95,244,245 — 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.

Table 3: Variable Symptoms and Signs of MS



Depressed mood


Memory loss/cognitive changes


Dizziness or vertigo

Decreased sensation (pain, vibration, position)


Decreased strength

Hearing loss and tinnitus

Hyperreflexia, spasticity

Heat sensitivity (Uhthoff Phenomenon)


Incoordination and gait disturbances

Lhermitte’s sign

Sensory disturbances (dysesthesias, numbness, paresthesia’s)

Visual defects (internuclear ophthalmoplegia, optic disc pallor, red color desaturation, reduced visual acuity)



Urinary symptoms


Visual disturbances (diplopia, oscillopsia)




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 carcinomatosis253,254,255,256 — 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


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.

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:

  • Inconclusive or show a need for additional or follow up imaging evaluation OR
  • The office notes should clearly document an indication why overlapping imaging is needed and how it will change management for the patient.

(*Unless approvable in the combination section as noted in the guidelines)

For evaluation of headache1,2,3,4,5

Chronic headache with a change in character/pattern (e.g., more frequent, increased severity, or duration)

  • Cluster headaches or other trigeminal-autonomic cephalgias, i.e., paroxysmal hemicrania, hemicrania continua, short-lasting unilateral neuralgiform headache attacks (SUNCT/SUNA) imaging is indicated once to eliminate secondary causes6
  • Acute headache, sudden onset:
    • With a personal or family history (brother, sister, parent, or child) of brain aneurysm or AVM (arteriovenous malformation) OR
    • < 48 hours of “worst headache in my life” or “thunderclap” headache.
      • Note: The duration of a thunderclap type headache lasts more than 5 minutes. Sudden onset new headache reaching maximum intensity within 2-3 minutes.
    • Prior history of stroke or intracranial bleed
    • Known coagulopathy or on anticoagulation
  • New onset of headache with any of the following:1,7,8
    • Acute, new, or fluctuating neurologic deficits, such as sensory deficits, limb weakness, abnormal reflexes (pathological, asymmetric, hyperreflexia), speech difficulties, visual loss, lack of coordination, or mental status changes or with signs of increased intracranial pressure (papilledema). (See background)
    • History of cancer or significantly immunocompromised
    • Fever
    • Subacute head trauma
    • Pregnancy or puerperium9,10
    • Age > 501,7,11,12,13
    • Severe unilateral headache with radiation to or from the neck, associated with suspicion of carotid or vertebral artery dissection
    • Related to activity or event (sexual activity, exertion, Valsalva, position), new or progressively worsening14
    • Persistent or progressively worsening during a course of physician-directed treatment1,15,16

Note: Neuroimaging warranted for atypical/complex migraine aura, but not for a typical migraine aura (see background)

  • Special considerations in the pediatric population with persistent headache:17,18,19
    • Occipital location
    • Age < 6 years
    • Symptoms indicative of increased intracranial pressure, such as recurring headaches after waking with or without associated nausea/vomiting
    • Documented absence of family history of headache
    • Severe headache in a child with an underlying disease that predisposes to intracranial pathology (e.g., immune deficiency, sickle cell disease, neurofibromatosis, history of neoplasm, coagulopathy, hypertension, congenital heart disease)

For evaluation of neurologic symptoms or deficits20

  • Acute, new, or fluctuating neurologic symptoms or deficits such as, sensory deficits, limb weakness, abnormal reflexes (pathological, asymmetric, hyperreflexia), speech difficulties, visual loss, lack of coordination, or mental status changes (see Background)

For evaluation of known or suspected stroke or vascular disease21,22,23

  • Known or suspected stroke with any acute, new, or fluctuating symptoms or deficits such as sensory deficits, limb weakness, speech difficulties, visual loss, lack of coordination, or mental status changes (see background)
  • Suspected stroke with a personal or first-degree family history (brother, sister, parent, or child) of aneurysm or known coagulopathy or on anticoagulation
  • Symptoms of transient ischemic attack (TIA) (episodic neurologic symptoms such as sensory deficits, limb weakness, speech difficulties, visual loss, lack of coordination, or mental status changes)
  • Evaluation of suspected acute subarachnoid hemorrhage (SAH)
  • Follow-up for known hemorrhage, hematoma, or vascular abnormalities

Note: MRI is the study of choice for detecting cavernous malformations (CCM) and other low flow vascular malformations (see background). Follow-up imaging of known CCM should be done only to guide treatment decisions or to investigate new symptoms. First-degree relatives of patients with more than one family member with a CCM should have a screening MRI as well as genetic counseling24,25,26

  • Suspected central venous thrombosis — See Background21,27
  • Screening for silent cerebral infarcts in early school age children and adults with HbSS sickle cell disease or HbSβ0 thalassemia28
  • Evaluation of neurological signs or symptoms in sickle cell disease29,30
  • High stroke risk in sickle cell patients (2 – 16 years of age) with a transcranial doppler velocity > 20031,32

For evaluation of known or suspected trauma33,34,35

  • Known or suspected trauma or injury to the head with documentation of one or more of the following acute, new, or fluctuating:
    • Focal neurologic findings
    • Motor changes
    • Mental status changes
    • Amnesia
    • Vomiting
    • Seizures
    • Headache
    • Signs of increased intracranial pressure
  • Known coagulopathy or on anticoagulation
  • Known or suspected skull fracture by physical exam and/or prior imaging
  • Post concussive syndrome if persistent or disabling symptoms and MRI has not been performed36
  • Subacute or chronic traumatic brain injury with new cognitive and/or neurologic deficit

For evaluation of suspected brain tumor, mass, or metastasis:37,3

  • Suspected brain tumor with any acute, new, or fluctuating neurologic symptoms or deficits such as sensory deficits, limb weakness, abnormal reflexes (pathological, asymmetric, hyperreflexia), speech difficulties, visual loss, lack of coordination, or mental status changes (see Background)

  • Suspected brain metastasis or intracranial involvement in patients with a history of cancer based on neurological symptoms or examination findings (may include new or changing lymph nodes)
  • Lesion with atypical features for further evaluation or follow up
  • Suspected Pituitary Tumors39,40,41,42
    • Neurologic findings (e.g., visual field deficit suggesting compression of the optic chiasm, diplopia, gaze palsy)
    • Suspected hypofunctioning pituitary gland based on hormonal testing
      • Hypopituitarism
      • Growth hormone deficiency
      • Hypogonadotropic hypogonadism [low sex hormones and gonadotropins (FSH/LH)]43
        • Total testosterone persistently < 150 with low or normal LH/FSH i.e., severe secondary hypogonadism OR
        • Total testosterone levels persistently borderline around the lower limits of normal range (200 – 400 ng/dL) with low or normal LH/FSH; AND
          • Neurological signs or symptoms; OR
          • Other pituitary hormonal abnormalities; OR
          • Low free testosterone and consideration and addressment of reversible functional causes of gonadotropin suppression (e.g., obesity, opioid use, diabetes, steroid use, or comorbid illness)
    • Suspected hyperfunctioning pituitary gland based on hormonal testing
      • Central hyperthyroidism (high TSH)
      • Cushing syndrome suspected (high ACTH (>5) with cortisol suppression on low or high dose dexamethasone suppression test)44,45,46,47
      • Acromegaly/gigantism (high GH/IGF-1)
      • Elevated prolactin48,49,50
        • ≥ 250 ng/mL OR
        • After evaluation for another cause (e.g., pregnancy, hypothyroidism, renal insufficiency, medication — See Background)
          • > 100 ng/mL OR
          • Persistently elevated OR
          • Neuroendocrine signs or symptoms (i.e., headache, galactorrhea, abnormal menses, infertility, or bitemporal hemianopsia) OR
          • Abnormal pituitary hormones (low testosterone/estrogen/ progesterone AND low or normal LH/FSH)
    • Central Diabetes Insipidus (low ADH)
    • Precocious puberty in a child (male < 9; female < 8), with hormonal studies suggesting a central cause51
    • Pituitary apoplexy with sudden onset of neurological and hormonal symptoms
  • For screening for known non-CNS Cancer52,53,54,55,56,57,58,59,60,61 — See Background
    • Default screening for
      • Kidney cancer
      • Lung cancer
      • Merkel cell carcinoma
      • Mucosal melanoma of the head and neck, especially of the oral cavity
      • Poorly differential neuroendocrine cancer (Large or Small cell/Unknown primary of neuroendocrine origin)
    • Screening with preconditions
      • AML….............................................................. Suspicion of leukemic meningitis
      • Cutaneous melanoma…................................. Stage IIIC or higher
      • Testicular cancer-Seminoma…....................... High risk
      • Gestational Trophoblastic Neoplasia…............ Pulmonary metastasis
      • Bladder cancer............................................... High risk, i.e., small cell
    • All other cancer if CNS symptoms present
  • Histiocytic Neoplasms for screening and/or with neurological signs or symptoms62,63
    • Erdheim-Chester Disease
    • Langerhans Cell Histiocytosis
    • Rosai-Dorfman Disease
  • For screening of Hereditary Cancer Syndromes — See Background
    • Li Fraumeni syndrome — Annually64
    • Von Hippel Lindau — Every 2 years, starting at age of 8 years65
    • Tuberous Sclerosis — Every 1 – 3 years, until the age of 25 years66
    • MEN1 — Every 3 – 5 years, starting at the age of 5 years67
    • NF 2 — Brain IAC: Annually starting at the age of 10 years68
    • Sturge Weber Syndrome: Once, after age 1 to rule out intracranial involvement; in patients < 1 year, only if symptomatic69

For evaluation of known brain tumor, mass, or metastasis

  • Follow-up of known CNS cancer (either primary malignant brain tumor or secondary brain metastasis) undergoing active treatment within the past year or as per surveillance imaging guidance for that cancer38
  • Suspected recurrence with prior history of CNS cancer based on neurological symptoms or examination findings
  • Follow-up of known low grade tumor (WHO I-II) (i.e., meningioma, glioma, astrocytoma, oligodendroglioma)
    • For surveillance as per professional society recommendations38
    • If symptomatic, new/changing signs or symptoms or complicating factors
  • Follow-up of known pituitary adenoma
    • New neuroendocrine signs or symptoms
    • Functioning adenoma - to assess response to treatment and 1-year follow-up after drug holiday70,71,72,73
    • Asymptomatic Macroadenoma (≥ 10mm) follow-up every 6 – 18 months, post-surgical follow-up every 1 – 2 years after surgery74
    • Asymptomatic, non-functioning Microadenoma < 10mm repeat in one year; if stable, repeat every 2 – 3 years75
  • Follow-up of known pineal cyst (> 5mm) if there are atypical features or symptoms (e.g., headaches, gaze paresis, ataxia, papilledema, nausea/vomiting)76,77
  • Follow up of known Rathke cleft cyst78,79
    • If no symptoms, MRI at 1/3/5 years to stability
    • With new neurological symptoms or atypical imaging features
    • Post treatment, yearly for 5 years
  • Follow-up of known arachnoid cyst80,81,82,83
    • In patients < 4 years old, serial imaging is warranted
    • In patients > 4 years old, repeat imaging only if newly symptomatic, i.e., headaches, increased intracranial pressure, hydrocephalus, local mass effect, seizures, visual/endocrine dysfunction
  • Midline dermoid cysts/sinuses with concern for intracranial extension41,42,43,48
  • Tumor monitoring in neurocutaneous syndromes as per tumor type
  • Histiocytic Neoplasms to assess treatment response and surveillance of known brain lesions62,63,84
    • Erdheim-Chester Disease
    • Langerhans Cell Histiocytosis
    • Rosai-Dorfman Disease

Indications for combination studies for the initial pre-therapy staging of cancer, OR active monitoring for recurrence as clinically indicated, OR evaluation of suspected metastases38

  • < 5 concurrent studies to include CT or MRI of any of the following areas as appropriate depending on the cancer: neck, abdomen, pelvis, chest, brain, cervical spine, thoracic spine or lumbar spine
For evaluation of known or suspected seizure disorder85,86,87,88,89,90
  • New onset of an unprovoked seizure
  • Newly identified change in seizure activity/pattern
  • Known seizure disorder without previous imaging
  • Medically refractory epilepsy

Note: In the pediatric population, imaging is not indicated in simple febrile seizures or in idiopathic focal or generalized epilepsy with typical features [BECTS, childhood absence epilepsy (CAE), juvenile absence epilepsy (JAE), and juvenile myoclonic epilepsy (JME)]87,91,92,93


For evaluation of suspected multiple sclerosis (MS)94,95,96,97

  • For evaluation of patient with neurologic symptoms or deficits suspicious for MS with:
    • A clinically isolated syndrome (optic neuritis, transverse myelitis, or brain stem syndrome); OR
    • Recurrent episodes of variable neurological signs or symptoms not attributable to another cause
  • To demonstrate dissemination in time for diagnosis (every 6-12 months)

For evaluation of known multiple sclerosis (MS)94,97,98

  • To establish a new baseline (no recent imaging, postpartum, or 3 – 6 months after switching disease modifying therapy)
  • Prior to starting or switching disease-modifying therapy
  • 6-month repeat scan in patients with MRI disease activity that is not associated with new clinical symptoms on a routine follow-up scan (i.e., Radiographically isolated syndrome)99
  • Every 1 – 2 years while on disease-modifying therapy to assess for subclinical disease activity, less frequently when stable for 2 – 3 years
  • New signs or symptoms suggested of an exacerbation or unexpected clinical worsening
  • Progressive Multifocal Leukoencephalopathy (PML) surveillance for patients on natalizumab (Tysabri)100
    • 12 months after the start of treatment in all patients
    • Further surveillance MRI scanning timing is based on risk
      • Annually, if anti-JCV antibody negative,
      • Every 3-4 months, if high risk of PML occurrence:
        • seropositive for JC virus and have been treated with natalizumab for ≥ 18 months OR
        • high anti-JC virus antibody index values (>0.9) OR
        • previously treated with immunosuppressive therapies
    • Brain MRI every 3 – 4 months for up to 12 months, in high-risk patients who switch from natalizumab to other therapeutics

Note: In the pediatric population, use a similar scan frequency for disease and therapeutic monitoring. Increase frequency of imaging (e.g., every 6 months) in children with highly active disease or in situations where imaging will change management.

For evaluation of known or suspected infectious or inflammatory disease (e.g., meningitis or abscess)101,102

  • Suspected intracranial abscess or brain infection with acute altered mental status or with positive lab findings (such as elevated WBCs) OR follow-up assessment during or after treatment completed
  • Meningitis with positive signs and symptoms (such as fever, headache, mental status changes, stiff neck) OR with positive lab findings (such as elevated white blood cells or abnormal lumbar puncture fluid exam)
  • Suspected encephalitis with headache and altered mental status or follow-up as clinically warranted
  • Endocarditis with suspected septic emboli
  • Suspected temporal arteritis in a patient > 50 with temporal headache, abrupt visual changes, jaw claudication, temporal artery tenderness, constitutional symptoms or elevated ESR;103,104,105,106,107 AND
    • Negative initial work-up (color Doppler ultrasonography or biopsy); OR
    • Atypical features, failure to response to treatment or concern for intracranial involvement

Note: Protocol should include high-resolution contrast-enhanced imaging the temporal artery

  • Central Nervous System (CNS) involvement in patients with known or suspected vasculitis or autoimmune disease with abnormal inflammatory markers or autoimmune antibodies
  • Suspected primary CNS vasculitis based on neurological signs and symptoms with completed infectious/inflammatory lab work-up108,109
  • Immunocompromised patient (e.g., transplant recipients, HIV with CD4<200, primary immunodeficiency syndromes, hematologic malignancies) with focal neurologic symptoms, headaches, behavioral, cognitive or personality changes
  • Neurosarcoidosis110,111,112
    • Initial Evaluation:
      • Suspected based on neurological sign/symptoms and lab work (ACE, CSF analysis) OR
      • Known history of sarcoidosis with neurological signs or symptoms
    • Follow-up of known neurosarcoidosis:
      • To assess treatment response
      • Worsening signs or symptoms

For evaluation of clinical assessment documenting cognitive impairment of unclear cause113,114,115

  • Mental status score of either MMSE or MoCA of less than 26 or other similar mental status instruments*/formal neuropsychological testing showing at least mild cognitive impairment AND a completed basic metabolic workup (such as thyroid function testing, liver function testing, complete blood count, electrolytes, and B12)

*Other examples include Mini-Cog, Memory Impairment Screen, Saint Louis University Mental Status Examination (SLUMS), Brief Alzheimer's Screen (BAS), Blessed Dementia Scale (BDS), Clinical Dementia Rating (CDR)116,117

FDA labeling for the drug Aduhelm (for Alzheimer’s disease) requires baseline imaging and monitoring

with brain MRI.118,119 Criteria for coverage includes the following:

  • Baseline study within 1 year of initiating treatment unless the patient has a more recent exacerbation, traumatic event [e.g., falls, etc.], or co-morbidity necessitating an evaluation within one-month preceding initiation
  • Prior to the 7th and 12th infusions
  • Monitoring if radiographic severe Amyloid Related Imaging Abnormalities (ARIA) is suspected or observed

NOTE: Enhanced clinical vigilance for ARIA is recommended during the first 8 doses of treatment with Aduhelm, particularly during titration. If a patient experiences symptoms which could be suggestive of ARIA, clinical evaluation should be performed, including MRI testing if indicated.

For evaluation of movement disorders120,121,122,123,124,125

  • For evaluation of suspected Parkinson’s with atypical feature or unresponsive to levodopa
  • For evaluation of new non-Parkinson neurological symptoms in known Parkinson’s diseasecomplicating the evaluation of the current condition
  • For the evaluation of other movement disorder to exclude a structural lesion (i.e., suspected Huntington disease, chorea, atypical parkinsonian syndromes, hemiballismus, atypical dystonia) Note: MRI not indicated in essential tremor, Tourette’ syndrome, or isolated focal dystonia (e.g., blepharospasm, cervical dystonia, laryngeal dystonia, oromandibular dystonia, writer’s dystonia)121,125,126

For evaluation of cranial nerve and visual abnormalities

  • Optic neuritis
  • Abnormal eye findings on physical or neurologic examination (papilledema, pathologic nystagmus, optic atrophy, ocular nerve palsies, new onset anisocoria, visual field deficit, etc.)127

Note: See Background

  • Binocular diplopia with concern for intracranial pathology128 after comprehensive eye evaluation129
  • Childhood strabismus with development delay or abnormal fundoscopic exam to rule out intracranial abnormalities130,131
  • Horner’s syndrome with symptoms localizing the lesion to the central nervous system132
  • Trigeminal neuralgia or neuropathy5,133,134
  • Occipital Neuralgia to exclude a structural lesion, notably in atypical cases135,136,137
  • Bell’s Palsy- if atypical signs, slow resolution beyond three weeks, no improvement at four months, or facial twitching/spasms prior to onset138
  • Hemifacial spasm139
  • Other objective cranial nerve palsy (CN IX-XII)140,141
  • Bulbar symptoms, i.e., difficulty in chewing, weakness of the facial muscles, dysarthria, palatal weakness, dysphagia, and dysphonia and/or signs, i.e., atrophy and fasciculations of the tongue and absent gag reflex142
  • Pseudobulbar symptoms, i.e., dysphagia, dysarthria, facial weakness, sudden, stereotyped emotional outbursts that are not reflective of mood and/or signs, i.e., spastic tongue and exaggerated gag/jaw jerk143

For evaluation of known or suspected congenital abnormality (such as craniosynostosis, neural tube defects)144,145

  • Known or suspected congenital abnormality with any acute, new, or fluctuating neurologic, motor, or mental status changes
  • Evaluation of macrocephaly in an infant/child <18 with previously abnormal US, abnormal neurodevelopmental examination, signs of increased ICP or closed anterior fontanelle146
  • Evaluation of microcephaly in an infant/child < 18
  • Evaluation of craniosynostosis and other skull deformities. CT is preferred imaging to assess bony structures; MRI imaging is preferred to assess intracranial soft tissue
  • Evaluation of the corticomedullary junction in Achondroplasia147,148
  • Cerebral palsy if etiology has not been established in the neonatal period, there is change in the expected clinical or developmental profile or concern for progressive neurological disorder149,150
  • X-linked Adrenoleukodystrophy151
    • Baseline MRI between 12 and 18 months old
    • Second MRI 1 year after baseline
    • MRI every 6 months between 3 and 12 years old
    • Annual MRI after 12 years old
  • Prior treatment OR treatment planned for congenital abnormality

Note: For evaluation of known or suspected hydrocephalus please see section on CSF abnormalities.

Cerebral Spinal Fluid (CSF) Abnormalities

  • Evaluation of suspected hydrocephalus with any acute, new, or fluctuating neurologic, motor, or mental status changes
  • Known hydrocephalus
  • For initial evaluation of a suspected Arnold Chiari malformation
  • Follow-up imaging of a known type II or type III Arnold Chiari malformation. For Arnold Chiari type I, follow-up imaging only if new or changing signs/symptoms152
  • Initial evaluation for a known syrinx or syringomyelia
  • Known or suspected normal pressure hydrocephalus (NPH)153
    • With symptoms of gait difficulty, cognitive disturbance, and urinary incontinence
  • Follow-up shunt evaluation154,155,156,157
    • Post operativity if indicated based on underlying disease or pre-operative radiographic findings and/or
    • 6 – 12 months after placement and/or
    • With neurologic symptoms that suggest shunt malfunction
  • Evaluation of known or suspected cerebrospinal fluid (CSF) leakage158
  • Cisternography for intermittent and complex CSF rhinorrhea/otorrhea. CSF fluid should always be confirmed with laboratory testing (Beta-2 transferrin assay)159,160
  • Suspected spontaneous intra-cranial hypotension with distinct postural headache (other symptoms include nausea, vomiting, dizziness, tinnitus, diplopia neck pain or imbalance)161,162
  • CSF flow study for evaluation and management of CSF flow disorders163, 164

Often congenital, but can present later in life; or less commonly acquired secondary to tumor, stroke, trauma, infection, etc.165

Pre-operative/procedural evaluation for brain/skull surgery

  • Pre-operative evaluation for a planned surgery or procedure

Post-operative/procedural evaluation

  • A follow-up study may be needed to help evaluate a patient’s progress after treatment, procedure, intervention, or surgery. Documentation requires a medical reason that clearly indicates why additional imaging is needed for the type and area(s) requested.

Further evaluation of indeterminate findings on prior imaging (unless follow up is otherwise specified within the guideline):

  • For initial evaluation of an inconclusive finding on a prior imaging report that requires further clarification.
  • One follow-up exam of a prior indeterminate MR/CT finding to ensure no suspicious interval change has occurred. (No further surveillance unless specified as highly suspicious or change was found on last follow-up exam)

Other Indications for a Brain MRI

  • Vertigo associated with any of the following166,167,168
    • Signs or symptoms suggestive of a CNS lesion (ataxia, visual loss, double vision, weakness, or a change in sensation)
    • Progressive unilateral hearing loss
    • Risk factors for cerebrovascular disease with concern for stroke
    • After full neurologic examination and vestibular testing with concern for central vertigo (i.e., skew deviation, vertical nystagmus, head thrust test, videonystagmography (VNG)/ electronystagmography (ENG))
  • Diagnosis of central sleep apnea on polysomnogram
    • Children > 1 year169
    • Adults in the absence of heart failure, chronic opioid use, high altitude, or treatment emergent central sleep apnea AND concern for a central neurological cause (Chiari malformation, tumor, infectious/inflammatory disease) OR with an abnormal neurological exam170
  • Syncope with clinical concern for seizure or associated neurological signs or symptoms171,172
  • Cyclical vomiting syndrome or abdominal migraine with any localizing neurological symptoms173,174,175
  • Soft tissue mass of the head with nondiagnostic initial evaluation (ultrasound and/or radiograph)176,177,178
  • Psychological changes with neurological deficits on exam or after completion of a full neurological assessment that suggests a possible neurologic cause179
  • Global developmental delay or developmental delay with abnormal neurological examination in a child < 18 years180,181
  • Unexplained event (BRUE) formerly apparent life-threatening event (ALTE) in infants < 1 year with concern for neurological cause based on history and exam182

Note: Imaging is not indicated in low-risk patients

  • Bone Marrow Transplant (BMT)
    • For initial workup of BMT (along with CT Chest183, CT Sinus and CT Abdomen and Pelvis)184

Indications for a Brain MRI with Internal Auditory Canal (IAC) (If only images of the IACs is needed w/o brain imaging see Guideline Number: NIA_CG_014)

  • Unilateral non-pulsatile tinnitus
  • Pulsatile tinnitus
  • Suspected acoustic neuroma (Schwannoma) or cerebellar pontine angle tumor with any of the following signs and symptoms: unilateral hearing loss by audiometry, headache, disturbed balance or gait, unilateral tinnitus, facial weakness, or altered sense of taste
  • Suspected cholesteatoma
  • Suspected glomus tumor
  • Asymmetric sensorineural hearing loss on audiogram
  • Congenital/childhood sensorineural hearing loss suspected to be due to a structural abnormality185,186,187 (CNVIII, the brain parenchyma, or the membranous labyrinth). CT is the preferred imaging modality for the osseous anatomy and malformations of the inner ear.
  • CSF otorrhea (MRI/Nuclear Cisternography for intermittent leaks, CT for active leaks)188; there should be a high suspicion or confirmatory CSF fluid laboratory testing (Beta-2 transferrin assay)
  • Clinical suspicion of acute mastoiditis as a complication of acute otitis media with intracranial complications (i.e., meningeal signs, cranial nerve deficits, focal neurological findings, altered mental status)189,190
  • Bell’s Palsy 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

Indications for MR Perfusion Imaging191

  • Neurovascular disease
    • Assessment of ischemic penumbra in acute stroke
    • Assessment of cerebrovascular reserve
    • Further evaluation of known vascular abnormality (stenosis, malformation, vasospasm, vasculitis, Moya-Moya)
  • Mass lesions
    • Differentiating tumor from tumor mimic
    • Differentiating glioblastoma from brain metastasis192
    • Discriminating low- from high-grade gliomas193
    • Differentiating recurrent brain tumors from radiation/chemo necrosis194,195
    • Surgical planning

Indications for Combination Studies21,22

Note: These body regions might be evaluated separately or in combination as documented in the clinical notes by physical examination findings (e.g., localization to a particular segment of the neuroaxis), patient history, and other available information, including prior imaging.

Exception: For approved indications as noted above and being performed in a child under 8 years of age who will need anesthesia for the procedure and there is a suspicion of concurrent intracranial pathology196

  • Brain MRI/Neck MRA*
    • Recent ischemic stroke or transient ischemic attack
    • Suspected carotid or vertebral artery dissection with focal or lateralizing neurological deficits
  • Brain MRI/Brain MRA*
    • Recent ischemic stroke or transient ischemic attack
    • Thunderclap headache with continued concern for underlying vascular abnormality after initial negative brain imaging > 6 hours after onset197,198,199

Note: Negative brain CT < 6 hours after headache onset excludes subarachnoid hemorrhage in neurologically intact patients200

    • Acute, sudden onset of headache with personal history of a vascular abnormality or first-degree family history of aneurysm
    • Headache associated with exercise, exertion, Valsalva or sexual activity6,14
    • Suspected venous thrombosis (dural sinus thrombosis) — Brain MRV — See Background
    • Neurological signs or symptoms in sickle cell patients
    • High stroke risk in sickle cell patients (2 – 16 years of age) with a transcranial doppler velocity > 20030
  • Brain MRI/Brain MRA/Neck MRA*
    • Recent stroke or transient ischemic attack (TIA)
    • Suspected carotid or vertebral artery dissection with focal or lateralizing neurological deficits
  • Brain MRI with IAC/ Brain MRA/Neck MRA (any combination)*
    • Pulsatile tinnitus with concern for a suspected arterial vascular and/or intracranial etiology201,202

*Note: MRA and CTA are generally comparable noninvasive imaging alternatives each with their own advantages and disadvantages. Brain MRI can alternatively be combined with Brain CTA/Neck CTA.

  • Brain MRI/Cervical MRI/Thoracic MRI (any combination)
    • Combination studies for MS: These body regions might be evaluated separately or in combination as guided by physical examination findings (e.g., localization to a particular segment of the spinal cord), patient history (e.g., symptom(s), time course, and where in the CNS the likely localization(s) is/are), and other available information, including prior imaging.
      • For evaluation of neuromyelitis optica spectrum disorders (recurrent or bilateral optic neuritis; recurrent transverse myelitis)203
      • For known MS, prior to the initiation or change of disease modification treatments and assess disease burden (to establish a new baseline)204
      • Follow-up scans, including brain and spine imaging, if patients have known spine disease:
  • 6 – 12 months after starting/changing treatment
  • Every 1 – 2 years while on disease-modifying therapy to assess for subclinical disease activity, less frequently when stable for 2 – 3 years
  • Brain MRI/Cervical MRI/Thoracic MRI/Lumbar MRI (any combination)
    • For initial evaluation of a suspected Arnold Chiari malformation
    • Follow-up imaging of a known type II or type III Arnold Chiari malformation. For Arnold Chiari type I, follow-up imaging only if new or changing signs/symptoms152,205
    • Oncological Applications (e.g., primary nervous system, metastatic)
      • Drop metastasis from brain or spine (see Background)
      • Suspected leptomeningeal carcinomatosis (see Background)206
      • Tumor evaluation and monitoring in neurocutaneous syndromes — See background
    • CSF leak highly suspected and supported by patient history and/or physical exam findings (known or suspected spontaneous (idiopathic) intracranial hypotension (SIH), post lumbar puncture headache, post spinal surgery headache, orthostatic headache, rhinorrhea or otorrhea, or cerebrospinal-venous fistula)
  • Brain MRI/Orbit MRI
    • Optic neuropathy or unilateral optic disk swelling of unclear etiology to distinguish between a compressive lesion of the optic nerve, optic neuritis, ischemic optic neuropathy (arteritic or non-arteritic), central retinal vein occlusion or optic nerve infiltrative disorders207
    • Bilateral optic disk swelling (papilledema) with visual loss208
    • Optic Neuritis
      • 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 retinoblastoma211,212
    • 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


  1. American College of Radiology. ACR Appropriateness Criteria® Headache. American College of Radiology. Updated 2022. Accessed January 23, 2023.
  2. Holle D, Obermann M. The role of neuroimaging in the diagnosis of headache disorders. Ther Adv Neurol Disord. Nov 2013;6(6):369-74. doi:10.1177/1756285613489765
  3. Quinones-Hinojosa A, Gulati M, Singh V, Lawton MT. Spontaneous intracerebral hemorrhage due to coagulation disorders. Neurosurg Focus. Oct 15 2003;15(4):E3. doi:10.3171/foc.2003.15.4.3
  4. Schaefer PW, Miller JC, Singhal AB, Thrall JH, Lee SI. Headache: when is neurologic imaging indicated? J Am Coll Radiol. Aug 2007;4(8):566-9. doi:10.1016/j.jacr.2006.10.001
  5. Wilbrink LA, Ferrari MD, Kruit MC, Haan J. Neuroimaging in trigeminal autonomic cephalgias: when, how, and of what? Curr Opin Neurol. Jun 2009;22(3):247-53. doi:10.1097/wco.0b013e32832b4bb3
  6. Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition. Cephalalgia. Jan 2018;38(1):1-211. doi:10.1177/0333102417738202
  7. Micieli A, Kingston W. An Approach to Identifying Headache Patients That Require Neuroimaging. Front Public Health. 2019;7:52. doi:10.3389/fpubh.2019.00052
  8. Mitsikostas DD, Ashina M, Craven A, et al. European Headache Federation consensus on technical investigation for primary headache disorders. J Headache Pain. 2015;17:5. doi:10.1186/s10194-016-0596-y
  9. Hamilton K. Secondary Headaches During Pregnancy and the Postpartum Period. BMC. Updated May 2020. Accessed January 23, 2023.
  10. Shobeiri E, Torabinejad B. Brain magnetic resonance imaging findings in postpartum headache. Neuroradiol J. Feb 2019;32(1):4-9. doi:10.1177/1971400918804193
  11. Nahas SJ. New Guidelines on Headache Imaging. NEJM Journal Watch. Updated January 8, 2020. Accessed January 23, 2023.
  12. D.W. D. Clinical clues and clinical rules: Primary vs secondary headache. Advanced Studies in Medicine. 2003;3(6C):S550-S555.
  13. Togha M, Karimitafti MJ, Ghorbani Z, et al. Characteristics and comorbidities of headache in patients over 50 years of age: a cross-sectional study. BMC Geriatrics. 2022/04/10 2022;22(1):313. doi:10.1186/s12877-022-03027-1
  14. Cordenier A, De Hertogh W, De Keyser J, Versijpt J. Headache associated with cough: a review. J Headache Pain. May 20 2013;14(1):42. doi:10.1186/1129-2377-14-42
  15. Kuruvilla DE, Lipton RB. Appropriate use of neuroimaging in headache. Curr Pain Headache Rep. Jun 2015;19(6):17. doi:10.1007/s11916-015-0490-3
  16. Martin VT. The diagnostic evaluation of secondary headache disorders. Headache. Feb 2011;51(2):346-52. doi:10.1111/j.1526-4610.2010.01841.x
  17. Gofshteyn JS, Stephenson DJ. Diagnosis and Management of Childhood Headache. Curr Probl Pediatr Adolesc Health Care. Feb 2016;46(2):36-51. doi:10.1016/j.cppeds.2015.11.003
  1. Dao JM, Qubty W. Headache Diagnosis in Children and Adolescents. Curr Pain Headache Rep. Feb 23 2018;22(3):17. doi:10.1007/s11916-018-0675-7
  2. Trofimova A, Vey BL, Mullins ME, Wolf DS, Kadom N. Imaging of Children With Nontraumatic Headaches. AJR Am J Roentgenol. Jan 2018;210(1):8-17. doi:10.2214/ajr.17.18561
  3. Wippold FJ, 2nd. Focal neurologic deficit. AJNR Am J Neuroradiol. Nov 2008;29(10):1998-2000.
  4. American College of Radiology. ACR Appropriateness Criteria®Cerebrovascular Disease. American College of Radiology (ACR). Updated 2016. Accessed January 22, 2023.
  5. American College of Radiology. ACR Appropriateness Criteria®Cerebrovascular Disease-Child. American College of Radiology (ACR). Updated 2019. Accessed January 23, 2023.
  6. Jauch EC, Saver JL, Adams HP, Jr., et al. Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. Mar 2013;44(3):870-947. doi:10.1161/STR.0b013e318284056a
  7. Akers A, Al-Shahi Salman R, I AA, et al. Synopsis of Guidelines for the Clinical Management of Cerebral Cavernous Malformations: Consensus Recommendations Based on Systematic Literature Review by the Angioma Alliance Scientific Advisory Board Clinical Experts Panel. Neurosurgery. May 1 2017;80(5):665-680. doi:10.1093/neuros/nyx091
  8. Velz J, Stienen MN, Neidert MC, Yang Y, Regli L, Bozinov O. Routinely Performed Serial Follow-Up Imaging in Asymptomatic Patients With Multiple Cerebral Cavernous Malformations Has No Influence on Surgical Decision Making. Front Neurol. 2018;9:848. doi:10.3389/fneur.2018.00848
  9. Zyck S, Gould GC. Cavernous Venous Malformation. StatPearls Publishing. Updated May 9, 2022. Accessed January 23, 2023.
  10. Bushnell C, Saposnik G. Evaluation and management of cerebral venous thrombosis. Continuum (Minneap Minn). Apr 2014;20(2 Cerebrovascular Disease):335-51. doi:10.1212/01.CON.0000446105.67173.a8
  11. DeBaun MR, Jordan LC, King AA, et al. American Society of Hematology 2020 guidelines for sickle cell disease: prevention, diagnosis, and treatment of cerebrovascular disease in children and adults. Blood Adv. Apr 28 2020;4(8):1554-1588. doi:10.1182/bloodadvances.2019001142
  12. Mackin RS, Insel P, Truran D, et al. Neuroimaging abnormalities in adults with sickle cell anemia: associations with cognition. Neurology. Mar 11 2014;82(10):835-41. doi:10.1212/wnl.0000000000000188
  13. Thust SC, Burke C, Siddiqui A. Neuroimaging findings in sickle cell disease. Br J Radiol. Aug 2014;87(1040):20130699. doi:10.1259/bjr.20130699
  14. Abboud MR, Cure J, Granger S, et al. Magnetic resonance angiography in children with sickle cell disease and abnormal transcranial Doppler ultrasonography findings enrolled in the STOP study. Blood. Apr 1 2004;103(7):2822-6. doi:10.1182/blood-2003-06-1972
  15. Sheehan VA, Hansbury EN, Smeltzer MP, Fortner G, McCarville MB, Aygun B. Transcranial Doppler velocity and brain MRI/MRA changes in children with sickle cell anemia on chronic transfusions to prevent primary stroke. Pediatr Blood Cancer. Sep 2013;60(9):1499-502. doi:10.1002/pbc.24569
  16. American College of Radiology. ACR Appropriateness Criteria® Head Trauma. American College of Radiology (ACR). Updated 2020. Accessed January 23, 2023.
  17. Jagoda AS, Bazarian JJ, Bruns JJ, Jr., et al. Clinical policy: neuroimaging and decisionmaking in adult mild traumatic brain injury in the acute setting. Ann Emerg Med. Dec 2008;52(6):714-48. doi:10.1016/j.annemergmed.2008.08.021
  18. Polinder S, Cnossen MC, Real RGL, et al. A Multidimensional Approach to Post-concussion Symptoms in Mild Traumatic Brain Injury. Front Neurol. 2018;9:1113. doi:10.3389/fneur.2018.01113
  19. Panwar J, Hsu CC, Tator CH, Mikulis D. Magnetic Resonance Imaging Criteria for Post-Concussion Syndrome: A Study of 127 Post-Concussion Syndrome Patients. J Neurotrauma. May 15 2020;37(10):1190-1196. doi:10.1089/neu.2019.6809
  20. Kernick DP, Ahmed F, Bahra A, et al. Imaging patients with suspected brain tumour: guidance for primary care. Br J Gen Pract. Dec 2008;58(557):880-5. doi:10.3399/bjgp08X376203
  21. NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines): Central Nervous System Cancers Version 2.2022. National Comprehensive Cancer Network (NCCN). Updated September 29, 2022. Accessed January 23, 2023.
  22. American College of Radiology. ACR Appropriateness Criteria® Neuroendocrine Imaging. American College of Radiology. Updated 2018. Accessed January 23, 2023.
  23. Consensus guidelines for the diagnosis and treatment of growth hormone (GH) deficiency in childhood and adolescence: summary statement of the GH Research Society. GH Research Society. J Clin Endocrinol Metab. Nov 2000;85(11):3990-3. doi:10.1210/jcem.85.11.6984
  24. Kannan S, Kennedy L. Diagnosis of acromegaly: state of the art. Expert Opin Med Diagn. Sep 2013;7(5):443-53. doi:10.1517/17530059.2013.820181
  25. Majumdar A, Mangal NS. Hyperprolactinemia. J Hum Reprod Sci. Jul 2013;6(3):168-75. doi:10.4103/0974-1208.121400
  26. Bhasin S, Brito JP, Cunningham GR, et al. Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. May 1 2018;103(5):1715-1744. doi:10.1210/jc.2018-00229
  27. Bonneville J-F, Potorac I, Petrossians P, Tshibanda L, Beckers A. Pituitary MRI in Cushing's disease - an update. Journal of Neuroendocrinology. 2022;34(8):e13123. doi:
  28. P. D, N.P. V. Dexamethasone Suppression Test. StatPearls Publishing Updated Aug 8 2022. Accessed April 7, 2023.
  29. L.K. N. Recent Updates on the Diagnosis and Management of Cushing's Syndrome. Endocrinol Metab. 2018;33(2):139-146.
  30. ARUP Consult aALtstfhp. Adrenal Hyperfunction (Cushing Syndrome) Testing Algorithm. ARUP Consult ( Updated May 2021. Accessed April 7, 2023.
  31. Melmed S, Casanueva FF, Hoffman AR, et al. Diagnosis and treatment of hyperprolactinemia: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. Feb 2011;96(2):273-88. doi:10.1210/jc.2010-1692
  32. Casanueva FF, Molitch ME, Schlechte JA, et al. Guidelines of the Pituitary Society for the diagnosis and management of prolactinomas. Clin Endocrinol (Oxf). Aug 2006;65(2):265-73. doi:10.1111/j.1365-2265.2006.02562.x
  33. Vilar L, Vilar CF, Lyra R, Freitas MDC. Pitfalls in the Diagnostic Evaluation of Hyperprolactinemia. Neuroendocrinology. 2019;109(1):7-19. doi:10.1159/000499694
  34. Faizah M, Zuhanis A, Rahmah R, et al. Precocious puberty in children: A review of imaging findings. Biomed Imaging Interv J. Jan 2012;8(1):e6. doi:10.2349/biij.8.1.e6
  35. NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines): Kidney Cancer Version 4.2023. National Comprehensive Cancer Network (NCCN). Updated January 18, 2023. Accessed January 23, 2023.
  36. NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines): Merkel Cell Carcinoma Version 2.2022. National Comprehensive Cancer Network (NCCN). Updated March 24, 2022. Accessed January 23, 2023.
  37. NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines): Melanoma: Cutaneous Version 1.2023. National Comprehensive Cancer Network (NCCN). Updated December 22, 2022. Accessed January 23, 2023.
  38. NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines): Melanoma: Uveal Version 2.2022. National Comprehensive Cancer Network (NCCN). Updated April 5, 2022. Accessed January 23, 2023.
  39. NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines): Non-Small Cell Lung Cancer Version 1.2023. National Comprehensive Cancer Network (NCCN). Updated December 22, 2022. Accessed January 23, 2023.
  40. NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines): Neuroendocrine and Adrenal Tumors Version 2.2022. National Comprehensive Cancer Network (NCCN). Updated December 21, 2022. Accessed January 23, 2023.
  41. NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines): Testicular Cancer Version 2.2022. National Comprehensive Cancer Network (NCCN). Updated January 4, 2022. Accessed January 23, 2023.
  42. NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines): Bladder Cancer Version 3.2022. National Comprehensive Cancer Network (NCCN). Updated December 21, 2022. Accessed January 23, 2023.
  43. NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines): Acute Myeloid Leukemia Version 3.2022. National Comprehensive Cancer Network (NCCN). Updated January 13, 2023. Accessed January 23, 2023.
  44. NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines): Gestational Trophoblastic Neoplasia Version 1.2023. National Comprehensive Cancer Network (NCCN). Updated December 20, 2022. Accessed January 23, 2023.
  45. Go RS, Jacobsen E, Baiocchi R, et al. Histiocytic Neoplasms, Version 2.2021, NCCN Clinical Practice Guidelines in Oncology. J Natl Compr Canc Netw. Nov 2021;19(11):1277-1303. doi:10.6004/jnccn.2021.0053
  1. Goyal G, Young JR, Koster MJ, et al. The Mayo Clinic Histiocytosis Working Group Consensus Statement for the Diagnosis and Evaluation of Adult Patients With Histiocytic Neoplasms: Erdheim-Chester Disease, Langerhans Cell Histiocytosis, and Rosai-Dorfman Disease. Mayo Clin Proc. Oct 2019;94(10):2054-2071. doi:10.1016/j.mayocp.2019.02.023
  2. Kumar P, Gill RM, Phelps A, Tulpule A, Matthay K, Nicolaides T. Surveillance Screening in Li-Fraumeni Syndrome: Raising Awareness of False Positives. Cureus. Apr 24 2018;10(4):e2527. doi:10.7759/cureus.2527
  3. Rednam SP, Erez A, Druker H, et al. Von Hippel-Lindau and Hereditary Pheochromocytoma/Paraganglioma Syndromes: Clinical Features, Genetics, and Surveillance Recommendations in Childhood. Clin Cancer Res. Jun 15 2017;23(12):e68-e75. doi:10.1158/1078-0432.Ccr-17-0547
  4. Krueger DA, Northrup H. Tuberous sclerosis complex surveillance and management: recommendations of the 2012 International Tuberous Sclerosis Complex Consensus Conference. Pediatr Neurol. Oct 2013;49(4):255-65. doi:10.1016/j.pediatrneurol.2013.08.002
  5. Brandi ML, Gagel RF, Angeli A, et al. Guidelines for diagnosis and therapy of MEN type 1 and type 2. J Clin Endocrinol Metab. Dec 2001;86(12):5658-71. doi:10.1210/jcem.86.12.8070
  6. Evans DGR, Salvador H, Chang VY, et al. Cancer and Central Nervous System Tumor Surveillance in Pediatric Neurofibromatosis 2 and Related Disorders. Clin Cancer Res. Jun 15 2017;23(12):e54-e61. doi:10.1158/1078-0432.Ccr-17-0590
  7. Comi AM. Presentation, diagnosis, pathophysiology, and treatment of the neurological features of Sturge-Weber syndrome. Neurologist. Jul 2011;17(4):179-84. doi:10.1097/NRL.0b013e318220c5b6
  8. Stoller JK, Nielsen C, Buccola J. Pituitary Tumor. Cleveland Clinic Intensive Review of Internal Medicine. 6th ed. Wolters Kluwer; 2015.
  9. Eroukhmanoff J, Tejedor I, Potorac I, et al. MRI follow-up is unnecessary in patients with macroprolactinomas and long-term normal prolactin levels on dopamine agonist treatment. Eur J Endocrinol. Mar 2017;176(3):323-328. doi:10.1530/eje-16-0897
  10. Kurosaki M, Kambe A, Watanabe T, Fujii S, Ogawa T. Serial 3 T magnetic resonance imaging during cabergoline treatment of macroprolactinomas. Neurol Res. Apr 2015;37(4):341-6. doi:10.1179/1743132814y.0000000457
  11. Varlamov EV, Hinojosa-Amaya JM, Fleseriu M. Magnetic resonance imaging in the management of prolactinomas; a review of the evidence. Pituitary. Feb 2020;23(1):16-26. doi:10.1007/s11102-019-01001-6
  12. Dekkers OM, Pereira AM, Romijn JA. Treatment and follow-up of clinically nonfunctioning pituitary macroadenomas. J Clin Endocrinol Metab. Oct 2008;93(10):3717-26. doi:10.1210/jc.2008-0643
  13. Lake MG, Krook LS, Cruz SV. Pituitary adenomas: an overview. Am Fam Physician. Sep 1 2013;88(5):319-27.
  14. Cauley KA, Linnell GJ, Braff SP, Filippi CG. Serial follow-up MRI of indeterminate cystic lesions of the pineal region: experience at a rural tertiary care referral center. AJR Am J Roentgenol. Aug 2009;193(2):533-7. doi:10.2214/ajr.08.1906
  15. Jussila MP, Olsén P, Salokorpi N, Suo-Palosaari M. Follow-up of pineal cysts in children: is it necessary? Neuroradiology. Dec 2017;59(12):1265-1273. doi:10.1007/s00234-017-1926-8
  1. Trifanescu R, Ansorge O, Wass JAH, Grossman AB, Karavitaki N. Rathke’s cleft cysts. Clinical Endocrinology. 2012;76(2):151-160. doi:
  2. Petersson M, Berinder K, Eden Engström B, et al. Natural history and surgical outcome of Rathke's cleft cysts—A study from the Swedish Pituitary Registry. Clinical Endocrinology. 2022;96(1):54-61. doi:
  3. Al-Holou WN, Yew AY, Boomsaad ZE, Garton HJ, Muraszko KM, Maher CO. Prevalence and natural history of arachnoid cysts in children. J Neurosurg Pediatr. Jun 2010;5(6):578-85. doi:10.3171/2010.2.Peds09464
  4. Al-Holou WN, Terman S, Kilburg C, Garton HJ, Muraszko KM, Maher CO. Prevalence and natural history of arachnoid cysts in adults. J Neurosurg. Feb 2013;118(2):222-31. doi:10.3171/2012.10.Jns12548
  5. Jafrani R, Raskin JS, Kaufman A, Lam S. Intracranial arachnoid cysts: Pediatric neurosurgery update. Surg Neurol Int. 2019;10:15. doi:10.4103/sni.sni_320_18
  6. Mustansir F, Bashir S, Darbar A. Management of Arachnoid Cysts: A Comprehensive Review. Cureus. Apr 10 2018;10(4):e2458. doi:10.7759/cureus.2458
  7. Haupt R, Minkov M, Astigarraga I, et al. Langerhans cell histiocytosis (LCH): guidelines for diagnosis, clinical work-up, and treatment for patients till the age of 18 years. Pediatr Blood Cancer. Feb 2013;60(2):175-84. doi:10.1002/pbc.24367
  8. American College of Radiology. ACR Appropriateness Criteria® Seizures and Epilepsy. American College of Radiology. Updated 2019. Accessed January 23, 2023.
  9. Cendes F, Theodore WH, Brinkmann BH, Sulc V, Cascino GD. Neuroimaging of epilepsy. Handb Clin Neurol. 2016;136:985-1014. doi:10.1016/b978-0-444-53486-6.00051-x
  10. Gaillard WD, Chiron C, Cross JH, et al. Guidelines for imaging infants and children with recent-onset epilepsy. Epilepsia. Sep 2009;50(9):2147-53. doi:10.1111/j.1528-1167.2009.02075.x
  11. Ho K, Lawn N, Bynevelt M, Lee J, Dunne J. Neuroimaging of first-ever seizure: Contribution of MRI if CT is normal. Neurol Clin Pract. Oct 2013;3(5):398-403. doi:10.1212/CPJ.0b013e3182a78f25
  12. Krumholz A, Wiebe S, Gronseth G, et al. Practice Parameter: evaluating an apparent unprovoked first seizure in adults (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Neurology. Nov 20 2007;69(21):1996-2007. doi:10.1212/01.wnl.0000285084.93652.43
  13. Ramli N, Rahmat K, Lim KS, Tan CT. Neuroimaging in refractory epilepsy. Current practice and evolving trends. Eur J Radiol. Sep 2015;84(9):1791-800. doi:10.1016/j.ejrad.2015.03.024
  14. Hourani R, Nasreddine W, Dirani M, et al. When Should a Brain MRI Be Performed in Children with New-Onset Seizures? Results of a Large Prospective Trial. American Journal of Neuroradiology. 2021;42(9):1695-1701. doi:10.3174/ajnr.A7193
  15. Hirtz D, Ashwal S, Berg A, et al. Practice parameter: evaluating a first nonfebrile seizure in children: report of the quality standards subcommittee of the American Academy of Neurology, The Child Neurology Society, and The American Epilepsy Society. Neurology. Sep 12 2000;55(5):616-23. doi:10.1212/wnl.55.5.616
  16. Bernasconi A, Cendes F, Theodore WH, et al. Recommendations for the use of structural magnetic resonance imaging in the care of patients with epilepsy: A consensus report from the International League Against Epilepsy Neuroimaging Task Force. Epilepsia. Jun 2019;60(6):1054-1068. doi:10.1111/epi.15612
  17. Consortium of Multiple Sclerosis Centers. 2018 MRI Protocol and Clinical Guidelines for MS. Consortium of Multiple Sclerosis Centers (CMSC). Updated May 22, 2018. Accessed January 23, 2023.
  18. Thompson AJ, Banwell BL, Barkhof F, et al. Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria. Lancet Neurol. Feb 2018;17(2):162-173. doi:10.1016/s1474-4422(17)30470-2
  19. Traboulsee A, Simon JH, Stone L, et al. Revised Recommendations of the Consortium of MS Centers Task Force for a Standardized MRI Protocol and Clinical Guidelines for the Diagnosis and Follow-Up of Multiple Sclerosis. AJNR Am J Neuroradiol. Mar 2016;37(3):394-401. doi:10.3174/ajnr.A4539
  20. Wattjes MP, Ciccarelli O, Reich DS, et al. 2021 MAGNIMS-CMSC-NAIMS consensus recommendations on the use of MRI in patients with multiple sclerosis. Lancet Neurol. Aug 2021;20(8):653-670. doi:10.1016/s1474-4422(21)00095-8
  21. Rae-Grant A, Day GS, Marrie RA, et al. Practice guideline recommendations summary: Disease-modifying therapies for adults with multiple sclerosis: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology. Neurology. Apr 24 2018;90(17):777-788. doi:10.1212/wnl.0000000000005347
  22. Amato MP, De Stefano N, Inglese M, et al. Secondary Prevention in Radiologically Isolated Syndromes and Prodromal Stages of Multiple Sclerosis. Review. Frontiers in Neurology. 2022-March-14 2022;13doi:10.3389/fneur.2022.787160
  23. McGuigan C, Craner M, Guadagno J, et al. Stratification and monitoring of natalizumab-associated progressive multifocal leukoencephalopathy risk: recommendations from an expert group. J Neurol Neurosurg Psychiatry. Feb 2016;87(2):117-25. doi:10.1136/jnnp-2015-311100
  24. Lummel N, Koch M, Klein M, Pfister HW, Brückmann H, Linn J. Spectrum and Prevalence of Pathological Intracranial Magnetic Resonance Imaging Findings in Acute Bacterial Meningitis. Clin Neuroradiol. Jun 2016;26(2):159-67. doi:10.1007/s00062-014-0339-x
  25. Oliveira CR, Morriss MC, Mistrot JG, Cantey JB, Doern CD, Sánchez PJ. Brain magnetic resonance imaging of infants with bacterial meningitis. J Pediatr. Jul 2014;165(1):134-9. doi:10.1016/j.jpeds.2014.02.061
  26. Diamantopoulos AP, Haugeberg G, Hetland H, Soldal DM, Bie R, Myklebust G. Diagnostic value of color Doppler ultrasonography of temporal arteries and large vessels in giant cell arteritis: a consecutive case series. Arthritis Care Res (Hoboken). Jan 2014;66(1):113-9. doi:10.1002/acr.22178
  27. D'Souza NM, Morgan ML, Almarzouqi SJ, Lee AG. Magnetic resonance imaging findings in giant cell arteritis. Eye (Lond). May 2016;30(5):758-62. doi:10.1038/eye.2016.19
  28. Klink T, Geiger J, Both M, et al. Giant cell arteritis: diagnostic accuracy of MR imaging of superficial cranial arteries in initial diagnosis-results from a multicenter trial. Radiology. Dec 2014;273(3):844-52. doi:10.1148/radiol.14140056
  29. Salehi-Abari I. 2016 ACR revised criteria for early diagnosis of giant cell (temporal) arteritis. Autoimmune Dis Ther Approaches Open Access. 2016;3:1-4.
  30. Yip A, Jernberg ET, Bardi M, et al. Magnetic resonance imaging compared to ultrasonography in giant cell arteritis: a cross-sectional study. Arthritis Res Ther. Oct 19 2020;22(1):247. doi:10.1186/s13075-020-02335-4
  1. Zuccoli G, Pipitone N, Haldipur A, Brown RD, Jr., Hunder G, Salvarani C. Imaging findings in primary central nervous system vasculitis. Clin Exp Rheumatol. Jan-Feb 2011;29(1 Suppl 64):S104-9.
  2. Godasi R, Pang G, Chauhan S, Bollu PC. Primary Central Nervous System Vasculitis. StatPearls Publishing. Updated October 12, 2022. Accessed January 23, 2023.
  3. Voortman M, Drent M, Baughman RP. Management of neurosarcoidosis: a clinical challenge. Curr Opin Neurol. Jun 2019;32(3):475-483. doi:10.1097/wco.0000000000000684
  4. Fritz D, van de Beek D, Brouwer MC. Clinical features, treatment and outcome in neurosarcoidosis: systematic review and meta-analysis. BMC Neurol. Nov 15 2016;16(1):220. doi:10.1186/s12883-016-0741-x
  5. Shah R, Roberson GH, Curé JK. Correlation of MR imaging findings and clinical manifestations in neurosarcoidosis. AJNR Am J Neuroradiol. May 2009;30(5):953-61. doi:10.3174/ajnr.A1470
  6. Harvey PD. Clinical applications of neuropsychological assessment. Dialogues Clin Neurosci. Mar 2012;14(1):91-9. doi:10.31887/DCNS.2012.14.1/pharvey
  7. Health Quality Ontario. The appropriate use of neuroimaging in the diagnostic work-up of dementia: an evidence-based analysis. Ont Health Technol Assess Ser. 2014;14(1):1-64.
  8. Narayanan L, Murray AD. What can imaging tell us about cognitive impairment and dementia? World J Radiol. Mar 28 2016;8(3):240-54. doi:10.4329/wjr.v8.i3.240
  9. Carpenter CR, Bassett ER, Fischer GM, Shirshekan J, Galvin JE, Morris JC. Four sensitive screening tools to detect cognitive dysfunction in geriatric emergency department patients: brief Alzheimer's Screen, Short Blessed Test, Ottawa 3DY, and the caregiver-completed AD8. Acad Emerg Med. Apr 2011;18(4):374-84. doi:10.1111/j.1553-2712.2011.01040.x
  10. McDougall GJ. A review of screening instruments for assessing cognition and mental status in older adults. Nurse Pract. Nov 1990;15(11):18-28.
  11. U.S. Food & Drug Administration. Reference ID: 4807032 Full Prescribing Information ADUHELM(tm). U.S. Food & Drug Administration. Updated June 2021. Accessed January 23, 2023.
  12. Inc. B. Aduhelm™ [prescribing information] Biogen Inc. 2023. Updated February 2023. 2023.
  13. American College of Radiology. ACR Appropriateness Criteria® Movement Disorders and Neurodegenerative Diseases. American College of Radiology. Updated 2019. Accessed January 23, 2023.
  14. Albanese A, Asmus F, Bhatia KP, et al. EFNS guidelines on diagnosis and treatment of primary dystonias. Eur J Neurol. Jan 2011;18(1):5-18. doi:10.1111/j.1468-1331.2010.03042.x
  15. Mascalchi M, Vella A, Ceravolo R. Movement disorders: role of imaging in diagnosis. J Magn Reson Imaging. Feb 2012;35(2):239-56. doi:10.1002/jmri.22825
  16. McFarland NR. Diagnostic Approach to Atypical Parkinsonian Syndromes. Continuum (Minneap Minn). Aug 2016;22(4 Movement Disorders):1117-42. doi:10.1212/con.0000000000000348
  17. Pyatigorskaya N, Gallea C, Garcia-Lorenzo D, Vidailhet M, Lehericy S. A review of the use of magnetic resonance imaging in Parkinson's disease. Ther Adv Neurol Disord. Jul 2014;7(4):206-20. doi:10.1177/1756285613511507
  1. Sharifi S, Nederveen AJ, Booij J, van Rootselaar AF. Neuroimaging essentials in essential tremor: a systematic review. Neuroimage Clin. 2014;5:217-31. doi:10.1016/j.nicl.2014.05.003
  2. Comella CL, National Organization for Rare Disorders. Cervical Dystonia. National Organization for Rare Disorders (NORD). Updated 2019. Accessed January 23, 2023.
  3. Chang VA, Meyer DM, Meyer BC. Isolated Anisocoria as a Presenting Stroke Code Symptom is Unlikely to Result in Alteplase Administration. J Stroke Cerebrovasc Dis. Jan 2019;28(1):163-166. doi:10.1016/j.jstrokecerebrovasdis.2018.09.029
  4. Iliescu DA, Timaru CM, Alexe N, et al. Management of diplopia. Rom J Ophthalmol. Jul-Sep 2017;61(3):166-170. doi:10.22336/rjo.2017.31
  5. American Association for Pediatric Ophthalmology and Strabismus. Five things physicians and patients should question: Don’t routinely order neuro-imaging for all patients with double vision. Choosing Wisely Initiative ABIM Foundation. Updated May 29, 2019. Accessed January 23, 2023.
  6. Kadom N. Pediatric strabismus imaging. Curr Opin Ophthalmol. Sep 2008;19(5):371-8. doi:10.1097/ICU.0b013e328309f165
  7. Yoon L, Kim HY, Kwak MJ, et al. Utility of Magnetic Resonance Imaging (MRI) in Children With Strabismus. J Child Neurol. Sep 2019;34(10):574-581. doi:10.1177/0883073819846807
  8. Lee JH, Lee HK, Lee DH, Choi CG, Kim SJ, Suh DC. Neuroimaging strategies for three types of Horner syndrome with emphasis on anatomic location. AJR Am J Roentgenol. Jan 2007;188(1):W74-81. doi:10.2214/ajr.05.1588
  9. Bendtsen L, Zakrzewska JM, Abbott J, et al. European Academy of Neurology guideline on trigeminal neuralgia. Eur J Neurol. Jun 2019;26(6):831-849. doi:10.1111/ene.13950
  10. Cruccu G, Finnerup NB, Jensen TS, et al. Trigeminal neuralgia: New classification and diagnostic grading for practice and research. Neurology. Jul 12 2016;87(2):220-8. doi:10.1212/wnl.0000000000002840
  11. Garza I. Craniocervical junction schwannoma mimicking occipital neuralgia. Headache. Sep 2007;47(8):1204-5. doi:10.1111/j.1526-4610.2007.00887.x
  12. Choi I, Jeon SR. Neuralgias of the Head: Occipital Neuralgia. J Korean Med Sci. Apr 2016;31(4):479-88. doi:10.3346/jkms.2016.31.4.479
  13. Vanelderen P, Lataster A, Levy R, Mekhail N, Van Kleef M, Van Zundert J. 8. Occipital Neuralgia. Pain Practice. 2010;10(2):137-144. doi:
  14. Quesnel AM, Lindsay RW, Hadlock TA. When the bell tolls on Bell's palsy: finding occult malignancy in acute-onset facial paralysis. Am J Otolaryngol. Sep-Oct 2010;31(5):339-42. doi:10.1016/j.amjoto.2009.04.003
  15. Hermier M. Imaging of hemifacial spasm. Neurochirurgie. May 2018;64(2):117-123. doi:10.1016/j.neuchi.2018.01.005
  16. American College of Radiology. ACR Appropriateness Criteria® Cranial Neuropathy. American College of Radiology (ACR). Updated 2022. Accessed January 22, 2023.
  17. Mumtaz S, Jensen MB. Facial neuropathy with imaging enhancement of the facial nerve: a case report. Future Neurol. Nov 1 2014;9(6):571-576. doi:10.2217/fnl.14.55
  18. Yedavalli VS, Patil A, Shah P. Amyotrophic Lateral Sclerosis and its Mimics/Variants: A Comprehensive Review. J Clin Imaging Sci. 2018;8:53. doi:10.4103/jcis.JCIS_40_18
  19. King RR, Reiss JP. The epidemiology and pathophysiology of pseudobulbar affect and its association with neurodegeneration. Degener Neurol Neuromuscul Dis. 2013;3:23-31. doi:10.2147/dnnd.S34160
  20. Ashwal S, Michelson D, Plawner L, Dobyns WB. Practice parameter: Evaluation of the child with microcephaly (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology. Sep 15 2009;73(11):887-97. doi:10.1212/WNL.0b013e3181b783f7
  21. Vinocur DN, Medina LS. Imaging in the evaluation of children with suspected craniosynostosis. Evidence-based imaging in pediatrics. Springer; 2010:43-52.
  22. Tan AP, Mankad K, Gonçalves FG, Talenti G, Alexia E. Macrocephaly: Solving the Diagnostic Dilemma. Top Magn Reson Imaging. Aug 2018;27(4):197-217. doi:10.1097/rmr.0000000000000170
  23. Dougherty H, Shaunak M, Irving M, Thompson D, Cheung MS. Identification of Characteristic Neurological Complications in Infants with Achondroplasia by Routine MRI Screening. ESPE Abstracts. 2018;89
  24. Kubota T, Adachi M, Kitaoka T, et al. Clinical Practice Guidelines for Achondroplasia. Clin Pediatr Endocrinol. 2020;29(1):25-42. doi:10.1297/cpe.29.25
  25. Ashwal S, Russman BS, Blasco PA, et al. Practice parameter: diagnostic assessment of the child with cerebral palsy: report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology. Mar 23 2004;62(6):851-63. doi:10.1212/01.wnl.0000117981.35364.1b
  26. Cerebral palsy in under 25s: assessment and management National Institute for Health and Care Excellence (NICE). Updated January 25, 2017. Accessed January 23, 2023.
  27. Mallack EJ, Turk BR, Yan H, et al. MRI surveillance of boys with X-linked adrenoleukodystrophy identified by newborn screening: Meta-analysis and consensus guidelines. J Inherit Metab Dis. May 2021;44(3):728-739. doi:10.1002/jimd.12356
  28. Whitson WJ, Lane JR, Bauer DF, Durham SR. A prospective natural history study of nonoperatively managed Chiari I malformation: does follow-up MRI surveillance alter surgical decision making? J Neurosurg Pediatr. Aug 2015;16(2):159-66. doi:10.3171/2014.12.Peds14301
  29. Damasceno BP. Neuroimaging in normal pressure hydrocephalus. Dement Neuropsychol. Oct-Dec 2015;9(4):350-355. doi:10.1590/1980-57642015dn94000350
  30. Kamenova M, Rychen J, Guzman R, Mariani L, Soleman J. Yield of early postoperative computed tomography after frontal ventriculoperitoneal shunt placement. PLoS One. 2018;13(6):e0198752. doi:10.1371/journal.pone.0198752
  31. Pople IK. Hydrocephalus and shunts: what the neurologist should know. J Neurol Neurosurg Psychiatry. Sep 2002;73 Suppl 1(Suppl 1):i17-22.doi:10.1136/jnnp.73.suppl_1.i17
  32. Reddy GK, Bollam P, Caldito G. Long-term outcomes of ventriculoperitoneal shunt surgery in patients with hydrocephalus. World Neurosurg. Feb 2014;81(2):404-10. doi:10.1016/j.wneu.2013.01.096
  33. Wetzel JS, Heaner DP, Gabel BC, Tubbs RS, Chern JJ. Clinical evaluation and surveillance imaging of children with myelomeningocele and shunted hydrocephalus: a follow-up study. J Neurosurg Pediatr. Oct 19 2018;23(2):153-158. doi:10.3171/2018.7.Peds1826
  34. Severson M, Strecker-McGraw MK. Cerebrospinal Fluid Leak. StatPearls Publishing. Updated August 8, 2022. Accessed January 23, 2023.
  35. Mantur M, Łukaszewicz-Zając M, Mroczko B, et al. Cerebrospinal fluid leakage--reliable diagnostic methods. Clin Chim Acta. May 12 2011;412(11-12):837-40. doi:10.1016/j.cca.2011.02.017
  36. Selcuk H, Albayram S, Ozer H, et al. Intrathecal gadolinium-enhanced MR cisternography in the evaluation of CSF leakage. AJNR Am J Neuroradiol. Jan 2010;31(1):71-5. doi:10.3174/ajnr.A1788
  37. Gordon N. Spontaneous intracranial hypotension. Dev Med Child Neurol. Dec 2009;51(12):932-5. doi:10.1111/j.1469-8749.2009.03514.x
  38. Deline C, Schievink WI, National Organization for Rare Disorders. Spontaneous Intracranial Hypotension. National Organization for Rare Disorders (NORD). Updated September 1, 2020. Accessed January 23, 2023.
  39. Bradley WG, Jr. Magnetic Resonance Imaging of Normal Pressure Hydrocephalus. Semin Ultrasound CT MR. Apr 2016;37(2):120-8. doi:10.1053/j.sult.2016.01.005
  40. Mohammad SA, Osman NM, Ahmed KA. The value of CSF flow studies in the management of CSF disorders in children: a pictorial review. Insights Imaging. Jan 28 2019;10(1):3. doi:10.1186/s13244-019-0686-x
  41. National Organization for Rare Disorders. Chiari Malformations. National Organization for Rare Disorders (NORD). Updated 2014. Accessed January 23, 2023.
  42. Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker DE. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. Nov 2009;40(11):3504-10. doi:10.1161/strokeaha.109.551234
  43. Welgampola MS, Young AS, Pogson JM, Bradshaw AP, Halmagyi GM. Dizziness demystified. Pract Neurol. Dec 2019;19(6):492-501. doi:10.1136/practneurol-2019-002199
  44. Yamada S, Yasui K, Kawakami Y, Hasegawa Y, Katsuno M. DEFENSIVE Stroke Scale: Novel Diagnostic Tool for Predicting Posterior Circulation Infarction in the Emergency Department. J Stroke Cerebrovasc Dis. Jun 2019;28(6):1561-1570. doi:10.1016/j.jstrokecerebrovasdis.2019.03.005
  45. Felix O, Amaddeo A, Olmo Arroyo J, et al. Central sleep apnea in children: experience at a single center. Sleep Med. Sep 2016;25:24-28. doi:10.1016/j.sleep.2016.07.016
  46. Malhotra A, Owens RL. What is central sleep apnea? Respir Care. Sep 2010;55(9):1168-78.
  47. Al-Nsoor NM, Mhearat AS. Brain computed tomography in patients with syncope. Neurosciences (Riyadh). Apr 2010;15(2):105-9.
  48. Strickberger SA, Benson DW, Biaggioni I, et al. AHA/ACCF Scientific Statement on the evaluation of syncope: from the American Heart Association Councils on Clinical Cardiology, Cardiovascular Nursing, Cardiovascular Disease in the Young, and Stroke, and the Quality of Care and Outcomes Research Interdisciplinary Working Group; and the American College of Cardiology Foundation: in collaboration with the Heart Rhythm Society: endorsed by the American Autonomic Society. Circulation. Jan 17 2006;113(2):316-27. doi:10.1161/circulationaha.105.170274
  49. Venkatesan T, Levinthal DJ, Tarbell SE, et al. Guidelines on management of cyclic vomiting syndrome in adults by the American Neurogastroenterology and Motility Society and the Cyclic Vomiting Syndrome Association. Neurogastroenterol Motil. Jun 2019;31 Suppl 2(Suppl 2):e13604. doi:10.1111/nmo.13604
  50. Li BUK. Managing cyclic vomiting syndrome in children: beyond the guidelines. Eur J Pediatr. Oct 2018;177(10):1435-1442. doi:10.1007/s00431-018-3218-7
  51. Angus-Leppan H, Saatci D, Sutcliffe A, Guiloff RJ. Abdominal migraine. Bmj. Feb 19 2018;360:k179. doi:10.1136/bmj.k179
  52. American College of Radiology. ACR Appropriateness Criteria® Soft-Tissue Masses. American College of Radiology. Updated 2022. Accessed January 23, 2023.
  53. Kim HS, An JK, Woo JJ, Yoon RG. Superficially Palpable Masses of the Scalp and Face: A Pictorial Essay. Journal of the Korean Society of Radiology. 2019;80(2):283-293.
  54. Zhang J, Li Y, Zhao Y, Qiao J. CT and MRI of superficial solid tumors. Quant Imaging Med Surg. Mar 2018;8(2):232-251. doi:10.21037/qims.2018.03.03
  55. American College of Radiology. ACR Appropriateness Criteria® Acute Mental Status Change, Delirium, and New Onset Psychosis American College of Radiology. Updated 2018. Accessed January 23, 2023.
  56. Ali AS, Syed NP, Murthy GS, et al. Magnetic resonance imaging (MRI) evaluation of developmental delay in pediatric patients. J Clin Diagn Res. Jan 2015;9(1):Tc21-4. doi:10.7860/jcdr/2015/11921.5478
  57. Momen AA, Jelodar G, Dehdashti H. Brain magnetic resonance imaging findings in developmentally delayed children. Int J Pediatr. 2011;2011:386984. doi:10.1155/2011/386984
  58. Tieder JS, Bonkowsky JL, Etzel RA, et al. Brief Resolved Unexplained Events (Formerly Apparent Life-Threatening Events) and Evaluation of Lower-Risk Infants: Executive Summary. Pediatrics. May 2016;137(5)doi:10.1542/peds.2016-0591
  59. Gerull S, Medinger M, Heim D, Passweg J, Stern M. Evaluation of the Pretransplantation Workup before Allogeneic Transplantation. Biology of Blood and Marrow Transplantation. 2014/11/01/ 2014;20(11):1852-1856. doi:
  60. Kaste SC, Kaufman RA, Sunkara A, et al. Routine pre- and post-hematopoietic stem cell transplant computed tomography of the abdomen for detecting invasive fungal infection has limited value. Biol Blood Marrow Transplant. Jun 2015;21(6):1132-5. doi:10.1016/j.bbmt.2015.02.023
  61. Joshi VM, Navlekar SK, Kishore GR, Reddy KJ, Kumar EC. CT and MR imaging of the inner ear and brain in children with congenital sensorineural hearing loss. Radiographics. May-Jun 2012;32(3):683-98. doi:10.1148/rg.323115073
  62. Dewan K, Wippold FJ, 2nd, Lieu JE. Enlarged vestibular aqueduct in pediatric sensorineural hearing loss. Otolaryngol Head Neck Surg. Apr 2009;140(4):552-8. doi:10.1016/j.otohns.2008.12.035
  63. Ralli M, Rolesi R, Anzivino R, Turchetta R, Fetoni AR. Acquired sensorineural hearing loss in children: current research and therapeutic perspectives. Acta Otorhinolaryngol Ital. Dec 2017;37(6):500-508. Sordità infantile acquisita: stato dell’arte della ricerca e prospettive terapeutiche. doi:10.14639/0392-100x-1574
  1. Hiremath SB, Gautam AA, Sasindran V, Therakathu J, Benjamin G. Cerebrospinal fluid rhinorrhea and otorrhea: A multimodality imaging approach. Diagn Interv Imaging. Jan 2019;100(1):3-15. doi:10.1016/j.diii.2018.05.003
  2. Patel KM, Almutairi A, Mafee MF. Acute otomastoiditis and its complications: Role of imaging. Operative Techniques in Otolaryngology-Head and Neck Surgery. 2014/03/01 2014;25(1):21-28. doi:
  3. Platzek I, Kitzler HH, Gudziol V, Laniado M, Hahn G. Magnetic resonance imaging in acute mastoiditis. Acta Radiol Short Rep. Feb 2014;3(2):2047981614523415. doi:10.1177/2047981614523415
  4. Radiology ACo. ACR Appropriateness Criteria® ACR-ASNR-SPR Practice Parameter for the Performance of Intracranial Magnetic Resonance Perfusion Imaging. 2022. Updated 2022. Accessed April 26, 2023.
  5. Suh CH, Kim HS, Jung SC, Choi CG, Kim SJ. Perfusion MRI as a diagnostic biomarker for differentiating glioma from brain metastasis: a systematic review and meta-analysis. Eur Radiol. Sep 2018;28(9):3819-3831. doi:10.1007/s00330-018-5335-0
  6. Arevalo-Perez J, Peck KK, Young RJ, Holodny AI, Karimi S, Lyo JK. Dynamic Contrast-Enhanced Perfusion MRI and Diffusion-Weighted Imaging in Grading of Gliomas. J Neuroimaging. Sep-Oct 2015;25(5):792-8. doi:10.1111/jon.12239
  7. Metaweh NAK, Azab AO, El Basmy AAH, Mashhour KN, El Mahdy WM. Contrast-Enhanced Perfusion MR Imaging to Differentiate Between Recurrent/Residual Brain Neoplasms and Radiation Necrosis. Asian Pac J Cancer Prev. Apr 25 2018;19(4):941-948. doi:10.22034/apjcp.2018.19.4.941
  8. Wang L, Wei L, Wang J, et al. Evaluation of perfusion MRI value for tumor progression assessment after glioma radiotherapy: A systematic review and meta-analysis. Medicine (Baltimore). Dec 24 2020;99(52):e23766. doi:10.1097/md.0000000000023766
  9. Lawson GR. Controversy: Sedation of children for magnetic resonance imaging. Arch Dis Child. Feb 2000;82(2):150-3. doi:10.1136/adc.82.2.150
  10. Whitehead MT, Cardenas AM, Corey AS, et al. ACR Appropriateness Criteria® Headache. J Am Coll Radiol. Nov 2019;16(11s):S364-s377. doi:10.1016/j.jacr.2019.05.030
  11. Yeh YC, Fuh JL, Chen SP, Wang SJ. Clinical features, imaging findings and outcomes of headache associated with sexual activity. Cephalalgia. Nov 2010;30(11):1329-35. doi:10.1177/0333102410364675
  12. Yuan MK, Lai PH, Chen JY, et al. Detection of subarachnoid hemorrhage at acute and subacute/chronic stages: comparison of four magnetic resonance imaging pulse sequences and computed tomography. J Chin Med Assoc. Mar 2005;68(3):131-7. doi:10.1016/s1726-4901(09)70234-5
  13. Chen CY, Fuh JL. Evaluating thunderclap headache. Curr Opin Neurol. Jun 1 2021;34(3):356-362. doi:10.1097/wco.0000000000000917
  14. Pegge SAH, Steens SCA, Kunst HPM, Meijer FJA. Pulsatile Tinnitus: Differential Diagnosis and Radiological Work-Up. Curr Radiol Rep. 2017;5(1):5. doi:10.1007/s40134-017-0199-7
  15. Yew KS. Diagnostic approach to patients with tinnitus. Am Fam Physician. Jan 15 2014;89(2):106-13.
  1. Wingerchuk DM, Banwell B, Bennett JL, et al. International consensus diagnostic criteria for neuromyelitis optica spectrum disorders. Neurology. Jul 14 2015;85(2):177-89. doi:10.1212/wnl.0000000000001729
  2. Kaunzner UW, Gauthier SA. MRI in the assessment and monitoring of multiple sclerosis: an update on best practice. Ther Adv Neurol Disord. Jun 2017;10(6):247-261. doi:10.1177/1756285617708911
  3. Radic JAE, Cochrane DD. Choosing Wisely Canada: Pediatric Neurosurgery Recommendations. Paediatr Child Health. Sep 2018;23(6):383-387. doi:10.1093/pch/pxy012
  4. Shah LM, Salzman KL. Imaging of spinal metastatic disease. Int J Surg Oncol. 2011;2011:769753. doi:10.1155/2011/769753
  5. Behbehani R. Clinical approach to optic neuropathies. Clin Ophthalmol. Sep 2007;1(3):233-46.
  6. Margolin E. The swollen optic nerve: an approach to diagnosis and management. Pract Neurol. Aug 2019;19(4):302-309. doi:10.1136/practneurol-2018-002057
  7. Kaur K, Gurnani B, Devy N. Atypical optic neuritis - a case with a new surprise every visit. GMS Ophthalmol Cases. 2020;10:Doc11. doi:10.3205/oc000138
  8. Phuljhele S, Kedar S, Saxena R. Approach to optic neuritis: An update. Indian J Ophthalmol. Sep 2021;69(9):2266-2276. doi:10.4103/ijo.IJO_3415_20
  9. de Graaf P, Göricke S, Rodjan F, et al. Guidelines for imaging retinoblastoma: imaging principles and MRI standardization. Pediatr Radiol. Jan 2012;42(1):2-14. doi:10.1007/s00247-011-2201-5
  10. Razek AA, Elkhamary S. MRI of retinoblastoma. Br J Radiol. Sep 2011;84(1005):775-84. doi:10.1259/bjr/32022497
  11. Pakalniskis MG, Berg AD, Policeni BA, et al. The Many Faces of Granulomatosis With Polyangiitis: A Review of the Head and Neck Imaging Manifestations. AJR Am J Roentgenol. Dec 2015;205(6):W619-29. doi:10.2214/ajr.14.13864
  12. Hughes MA, Frederickson AM, Branstetter BF, Zhu X, Sekula RF, Jr. MRI of the Trigeminal Nerve in Patients With Trigeminal Neuralgia Secondary to Vascular Compression. AJR Am J Roentgenol. Mar 2016;206(3):595-600. doi:10.2214/ajr.14.14156
  13. Jang YE, Cho EY, Choi HY, Kim SM, Park HY. Diagnostic Neuroimaging in Headache Patients: A Systematic Review and Meta-Analysis. Psychiatry Investig. Jun 2019;16(6):407-417. doi:10.30773/pi.2019.04.11
  14. Spierings EL. Acute, subacute, and chronic headache. Otolaryngol Clin North Am. Dec 2003;36(6):1095-107, vi. doi:10.1016/s0030-6665(03)00128-2
  15. Tyagi A. New daily persistent headache. Ann Indian Acad Neurol. Aug 2012;15(Suppl 1):S62-5. doi:10.4103/0972-2327.100011
  16. Hadjikhani N, Vincent M. Neuroimaging clues of migraine aura. J Headache Pain. Apr 3 2019;20(1):32. doi:10.1186/s10194-019-0983-2
  17. Chhetri SK, Gow D, Shaunak S, Varma A. Clinical assessment of the sensory ataxias; diagnostic algorithm with illustrative cases. Pract Neurol. Aug 2014;14(4):242-51. doi:10.1136/practneurol-2013-000764
  18. Foster H, Drummond P, Jandial S, Clinch J, Wood M, Driscoll S. Evaluation of gait disorders in children. BMJ Best Practice. Updated February 23, 2021. Accessed January 23, 2023.
  19. Standford Medicine. Gait Abnormalities. Stanford University. Accessed January 23, 2023.
  20. Haynes KB, Wimberly RL, VanPelt JM, Jo CH, Riccio AI, Delgado MR. Toe Walking: A Neurological Perspective After Referral From Pediatric Orthopaedic Surgeons. J Pediatr Orthop. Mar 2018;38(3):152-156. doi:10.1097/bpo.0000000000001115
  21. Marshall FJ. Approach to the elderly patient with gait disturbance. Neurol Clin Pract. Jun 2012;2(2):103-111. doi:10.1212/CPJ.0b013e31825a7823
  22. Pirker W, Katzenschlager R. Gait disorders in adults and the elderly : A clinical guide. Wien Klin Wochenschr. Feb 2017;129(3-4):81-95. doi:10.1007/s00508-016-1096-4
  23. Sacco RL, Kasner SE, Broderick JP, et al. An updated definition of stroke for the 21st century: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. Jul 2013;44(7):2064-89. doi:10.1161/STR.0b013e318296aeca
  24. Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. Jul 2014;45(7):2160-236. doi:10.1161/str.0000000000000024
  25. Easton JD, Saver JL, Albers GW, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke. Jun 2009;40(6):2276-93. doi:10.1161/strokeaha.108.192218
  26. Hong KS, Yegiaian S, Lee M, Lee J, Saver JL. Declining stroke and vascular event recurrence rates in secondary prevention trials over the past 50 years and consequences for current trial design. Circulation. May 17 2011;123(19):2111-9. doi:10.1161/circulationaha.109.934786
  27. Wintermark M, Sanelli PC, Albers GW, et al. Imaging recommendations for acute stroke and transient ischemic attack patients: A joint statement by the American Society of Neuroradiology, the American College of Radiology, and the Society of NeuroInterventional Surgery. AJNR Am J Neuroradiol. Nov-Dec 2013;34(11):E117-27. doi:10.3174/ajnr.A3690
  28. Robertson RL, Palasis S, Rivkin MJ, et al. ACR Appropriateness Criteria® Cerebrovascular Disease-Child. J Am Coll Radiol. May 2020;17(5s):S36-s54. doi:10.1016/j.jacr.2020.01.036
  29. Salmela MB, Mortazavi S, Jagadeesan BD, et al. ACR Appropriateness Criteria(®) Cerebrovascular Disease. J Am Coll Radiol. May 2017;14(5s):S34-s61. doi:10.1016/j.jacr.2017.01.051
  30. Lee M, Kim MS. Image findings in brain developmental venous anomalies. J Cerebrovasc Endovasc Neurosurg. Mar 2012;14(1):37-43. doi:10.7461/jcen.2012.14.1.37
  31. Jensen RH, Radojicic A, Yri H. The diagnosis and management of idiopathic intracranial hypertension and the associated headache. Ther Adv Neurol Disord. Jul 2016;9(4):317-26. doi:10.1177/1756285616635987
  32. Connors JM, Levy JH. Thromboinflammation and the hypercoagulability of COVID-19. J Thromb Haemost. Jul 2020;18(7):1559-1561. doi:10.1111/jth.14849.
  1. Tu TM, Goh C, Tan YK, et al. Cerebral Venous Thrombosis in Patients with COVID-19 Infection: a Case Series and Systematic Review. J Stroke Cerebrovasc Dis. Dec 2020;29(12):105379. doi:10.1016/j.jstrokecerebrovasdis.2020.105379
  2. Coutinho JM. Cerebral venous thrombosis. J Thromb Haemost. Jun 2015;13 Suppl 1:S238-44. doi:10.1111/jth.12945
  3. Ferro JM, Canhão P, Aguiar de Sousa D. Cerebral venous thrombosis. Presse Med. Dec 2016;45(12 Pt 2):e429-e450. doi:10.1016/j.lpm.2016.10.007
  4. Atluri S, Sarathi V, Goel A, Boppana R, Shivaprasad C. Etiological Profile of Galactorrhoea. Indian J Endocrinol Metab. Jul-Aug 2018;22(4):489-493. doi:10.4103/ijem.IJEM_89_18
  5. Huang W, Molitch ME. Evaluation and management of galactorrhea. Am Fam Physician. Jun 1 2012;85(11):1073-80.
  6. Melmed S, Casanueva FF, Hoffman AR, et al. Diagnosis and Treatment of Hyperprolactinemia: An Endocrine Society Clinical Practice Guideline. The Journal of Clinical Endocrinology & Metabolism. 2011;96(2):273-288. doi:10.1210/jc.2010-1692
  7. Kamihara J, Bourdeaut F, Foulkes WD, et al. Retinoblastoma and Neuroblastoma Predisposition and Surveillance. Clin Cancer Res. Jul 1 2017;23(13):e98-e106. doi:10.1158/1078-0432.Ccr-17-0652
  8. Grasparil AD, Gottumukkala RV, Greer M-LC, Gee MS. Whole-Body MRI Surveillance of Cancer Predisposition Syndromes: Current Best Practice Guidelines for Use, Performance, and Interpretation. American Journal of Roentgenology. 2020/10/01 2020;215(4):1002-1011. doi:10.2214/AJR.19.22399
  9. Borofsky S, Levy LM. Neurofibromatosis: types 1 and 2. AJNR Am J Neuroradiol. Dec 2013;34(12):2250-1. doi:10.3174/ajnr.A3534
  10. Rovira À, Wattjes MP, Tintoré M, et al. Evidence-based guidelines: MAGNIMS consensus guidelines on the use of MRI in multiple sclerosis-clinical implementation in the diagnostic process. Nat Rev Neurol. Aug 2015;11(8):471-82. doi:10.1038/nrneurol.2015.106
  11. Saguil A, Kane S, Farnell E. Multiple sclerosis: a primary care perspective. Am Fam Physician. Nov 1 2014;90(9):644-52.
  12. Larivière D, Sacre K, Klein I, et al. Extra- and intracranial cerebral vasculitis in giant cell arteritis: an observational study. Medicine (Baltimore). Dec 2014;93(28):e265. doi:10.1097/md.0000000000000265
  13. Geyer M, Nilssen E. Evidence-based management of a patient with anosmia. Clin Otolaryngol. Oct 2008;33(5):466-9. doi:10.1111/j.1749-4486.2008.01819.x
  14. Lechien JR, Chiesa-Estomba CM, De Siati DR, et al. Olfactory and gustatory dysfunctions as a clinical presentation of mild-to-moderate forms of the coronavirus disease (COVID-19): a multicenter European study. Eur Arch Otorhinolaryngol. Aug 2020;277(8):2251-2261. doi:10.1007/s00405-020-05965-1
  15. Saniasiaya J, Islam MA, Abdullah B. Prevalence of Olfactory Dysfunction in Coronavirus Disease 2019 (COVID-19): A Meta-analysis of 27,492 Patients. Laryngoscope. Apr 2021;131(4):865-878. doi:10.1002/lary.29286
  16. Smith R, Leonidas JC, Maytal J. The value of head ultrasound in infants with macrocephaly. Pediatr Radiol. Mar 1998;28(3):143-6. doi:10.1007/s002470050315
  17. Pindrik J, Ye X, Ji BG, Pendleton C, Ahn ES. Anterior fontanelle closure and size in full-term children based on head computed tomography. Clin Pediatr (Phila). Oct 2014;53(12):1149-57. doi:10.1177/0009922814538492
  1. Cooper AS, Friedlaender E, Levy SE, et al. The Implications of Brain MRI in Autism Spectrum Disorder. J Child Neurol. Dec 2016;31(14):1611-1616. doi:10.1177/0883073816665548
  2. Andersen BM, Miranda C, Hatzoglou V, DeAngelis LM, Miller AM. Leptomeningeal metastases in glioma: The Memorial Sloan Kettering Cancer Center experience. Neurology. May 21 2019;92(21):e2483-e2491. doi:10.1212/wnl.0000000000007529
  3. Clarke JL, Perez HR, Jacks LM, Panageas KS, Deangelis LM. Leptomeningeal metastases in the MRI era. Neurology. May 4 2010;74(18):1449-54. doi:10.1212/WNL.0b013e3181dc1a69
  4. Maillie L, Salgado LR, Lazarev S. A systematic review of craniospinal irradiation for leptomeningeal disease: past, present, and future. Clin Transl Oncol. Oct 2021;23(10):2109-2119. doi:10.1007/s12094-021-02615-8
  5. Wang N, Bertalan MS, Brastianos PK. Leptomeningeal metastasis from systemic cancer: Review and update on management. Cancer. Jan 1 2018;124(1):21-35. doi:10.1002/cncr.30911
  6. Ahmed A. MRI features of disseminated 'drop metastases'. S Afr Med J. Jul 2008;98(7):522-3.


  1. Radmanesh A, Raz E, Zan E, Derman A, Kaminetzky M. Brain Imaging Use and Findings in COVID-19: A Single Academic Center Experience in the Epicenter of Disease in the United States. AJNR Am J Neuroradiol. Jul 2020;41(7):1179-1183. doi:10.3174/ajnr.A6610
  2. Naelitz B, Shah A, Nowacki AS, et al. Prolactin-to-Testosterone Ratio Predicts Pituitary Abnormalities in Mildly Hyperprolactinemic Men with Symptoms of Hypogonadism. J Urol. 2021;205(3):871-878. doi:10.1097/JU.0000000000001431

Coding Section 

Code Number Description
CPT 70540 Magnetic resonance (e.g., proton) imaging, orbit, face, and/or neck; without contrast material(s)
  70542 Magnetic resonance (e.g., proton) imaging, orbit, face, and/or neck; with contrast material(s)
  70543 Magnetic resonance (e.g., proton) imaging, orbit, face, and/or neck; without contrast material(s), followed by contrast material(s) and further sequences
  70551 Magnetic resonance (e.g., proton) imaging, brain (including brain stem); without contrast material
  70552 Magnetic resonance (e.g., proton) imaging, brain (including brain stem); with contrast material(s)
  70553 Magnetic resonance (e.g., proton) imaging, brain (including brain stem); without contrast material, followed by contrast material(s) and further sequences

Quantitative magnetic resonance for analysis of tissue composition (eg, fat, iron, water content), including multiparametric data acquisition, data preparation and transmission, interpretation and report, obtained without diagnostic mri examination of the same anatomy (eg, organ, gland, tissue, target structure) during the same session; multiple organs (list separately in addition to code for  primary procedure)                                                           

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.

"Current Procedural Terminology © American Medical Association. All Rights Reserved" 

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