CT Head/Brain - CAM 742

Description
Computed tomography (CT) is an imaging technique used to view the structures of the brain and is useful in evaluating pathologies in the brain. It provides more detailed information on head trauma, brain tumors, stroke, and other pathologies in the brain than regular radiographs.

CT scan 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 individuals with headache disorders along with abnormal neurologic examination results or predisposing factors for brain pathology.

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 individual 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.1,6,104,105,106

Migraine with aura6,7,107 — 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 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 brain stem, 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 or CT 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.

Imaging for stroke — Individuals presenting with symptoms of acute stroke should receive prompt imaging to determine whether they are candidates for treatment with tissue plasminogen activator. Non-contrast CT can evaluate for hemorrhage that would exclude the individual from reperfusion therapy. Functional imaging can be used to select individuals for thrombolytic therapy by measuring the mismatch between “infarct core” and “ischemic penumbra” and may define ischemic areas of the brain with the potential to respond positively to reperfusion therapy. Contrast-enhanced CT angiography (CTA) may follow the non-contrast CT imaging to identify areas of large vessel stenosis or occlusion which may be a target for therapy.

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.”108 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.109 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.”110 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.111
 
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 and to assess immediate complications and risk of future stroke. The majority of stoke evaluations take place in the inpatient setting. Admitting TIA individuals 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.110 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.109 Diagnostic recommendations include neuroimaging evaluation as soon as possible, preferably with MRI, including DWI; noninvasive imaging of the extracranial vessels should be performed; and noninvasive imaging of intracranial vessels is reasonable.112

Individuals with a history of stroke and recent workup 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.

CT and central venous thrombosis — A CTV or MRV 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),113 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. Since venous thrombosis can cause SAH, infarctions, and hemorrhage, parenchymal imaging with MRI/CT is also appropriate.16,114,115

CT scan for head trauma — Most types of head injury are minor injuries; clinical signs and symptoms help predict the need for brain CT following injury. CT has advantages in evaluating head injury due to its sensitivity for demonstrating mass effect, ventricular size and configuration, bone injuries, and acute hemorrhage. An individual who presents with certain clinical risk factors may be more likely to benefit from CT imaging. Some of the clinical risk factors that may be used as a guide to predict the probability of abnormal CT following minor head injury are vomiting, skull fracture, and age greater than 60 years. Individuals with a Glasgow Coma Scale of 15 or less who also have been vomiting or have a suspected skull fracture are likely to show abnormal results on CT scan. CT is also useful in detecting delayed hematoma, hypoxic-ischemic lesions, or cerebral edema in the first 72 hours after head injury.

CT and tumors — MRI is the ideal modality to follow-up meningioma, pituitary tumors, low grade tumors, neurocutaneous syndromes, and staging/surveillance for non-CNS cancers. CT should only be used when MRI is contraindicated or is unable to be obtained. Surveillance timelines should follow NCCN guidelines. Imaging is also warranted if the individual is symptomatic or there are new/changing signs or symptoms or complicating factors.
 
MMSE — The Mini Mental State Examination (MMSE) is a tool that can systematically and thoroughly assess mental status. 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.

CT for evaluation of the cranial nerves — Magnetic resonance imaging (MRI) is considered the gold standard in the study and evaluation of the cranial nerves. Computed tomography (CT) allows, usually, an indirect view of the nerve and is useful to demonstrate the intraosseous segments of cranial nerves, the foramina through which they exit skull base, and their pathologic changes. In optic neuritis, CT has limited utility. Contrast-enhanced CT scanning of the orbits may help exclude other orbital pathology. CT scanning of the brain, regardless of whether intravenous contrast material is administered or not, does not yield prognostic and treatment-altering information. In Bell’s Palsy temporal bone CT is useful in the evaluation of the caliber and the course of the IAC and bony facial nerve canal in the temporal bone. When using CT to evaluate the facial nerve, pathology often can only be inferred by visualization of erosion or destruction of the adjacent bony facial nerve canal. In contrast, MRI visualizes soft tissues well and so is better suited for evaluating soft tissue facial nerve abnormalities.

Anosmia — There is no relevant literature to support the use of CT head in the evaluation of the olfactory nerve.

CT scan for congenital abnormalities — While MRI is preferred to CT for evaluation of most congenital CNS abnormalities, in some clinical situations CT is preferred (craniosynostosis) or equivalent to MRI. CT is appropriate in the follow-up of hydrocephalus or VP shunt function where the etiology of hydrocephalus has been previously determined or in individuals for which MRI evaluation would require general anesthesia.

CT 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.116 The anterior fontanelle generally closes between 10 and 24 months of age, with 3% closing between 5 – 9 months and 11% after 24 months.117
 
CT 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.

CT 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.

CT 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.

CT scan and meningitis — In suspected bacterial meningitis, CT with contrast may be performed before lumbar puncture (LP) to show preliminary meningeal enhancement. It is important to evaluate for a mass lesion or cause of elevated ICP that would contraindicate an LP. CT may be used to define the pathology of the base of the skull and that may require therapeutic intervention and surgical consultation. Some causes of an intracranial infection include fractures of the paranasal sinus and inner ear infection.

Leptomeningeal carcinomatosis118,119,120,121 — 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.122

General Information

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

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

Policy 
REDUCING RADIATION EXPOSURE
Brain CT/brain CTA are not approvable simultaneously unless they meet the criteria described below in the Indications for brain CT/brain CTA 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

Important Note: Brain MRI is preferred to brain CT in most circumstances where the patient can tolerate MRI and sufficient time is available to schedule the MRI examination. Assessment of subarachnoid hemorrhage, acute trauma, or bone abnormalities of the calvarium (fracture, etc.) may be better imaged with CT. CT is also appropriate in an urgent situation where MRI is not readily available (stroke, increased ICP, CNS infection).

‡‡Designates CT is indicated only when MRI is contraindicated or cannot be performed

INDICATIONS FOR BRAIN CT

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)
    • < 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
    • Age > 50‡‡
    • New 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) and (new or progressively worsening‡‡
    • Persistent or worsening during a course of physician-directed treatment1,9,10‡‡

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 headache11
    • 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 deficits12

  • 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 disease13,14,15

  • 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 first-degree family history of aneurysm (brother, sister, parent, or child) 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)‡‡
  • Suspected acute subarachnoid hemorrhage (SAH)
  • Follow-up for known hemorrhage, hematoma, or vascular abnormalities
  • Suspected central venous thrombosis - see background14,16‡‡
  • Evaluation of neurological signs or symptoms in sickle cell disease17,18,19‡‡
  • High stroke risk in sickle cell patients (2 – 16 years of age) with a transcranial doppler velocity > 200‡‡19

For evaluation of known or suspected trauma20,21,22,23,24

  • 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
  • Repeat scan 24 hours post head trauma for anticoagulated patients with suspected diagnosis of delayed subdural hematoma
  • Post concussive syndrome if persistent or disabling symptoms and imaging has not been performed
  • Subacute or chronic traumatic brain injury with new cognitive and/or neurologic deficit‡‡

For evaluation of suspected brain tumor, mass, or metastasis25,26,27

  • Suspected brain tumor with any acute, new, or fluctuating neurologic symptoms or deficits such as sensory deficits, abnormal reflexes (pathological, asymmetric, hyperreflexia), limb weakness, 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 symptoms or examination findings (may include new or changing lymph nodes)‡‡
  • Lesion with atypical features for further evaluation or follow up
  • Suspected Pituitary Tumors (Brain MRI is the study of choice if indicated) or sella CT if MRI is contraindicated or cannot be performed
  • Histiocytic Neoplasms for screening and/or with neurological signs or symptoms28,29
    • Erdheim-Chester Disease
    • Langerhans Cell Histiocytosis
    • Rosai-Dorfman Disease
  • Screening for known non-CNS Cancer and for screening of hereditary cancers syndromes (Brain MRI is the study of choice if indicated)

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 cancer27‡‡
  • Suspected recurrence with prior history of CNS cancer (either primary or secondary) 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 as per professional society recommendations27
    • If symptomatic, new/changing signs or symptoms or complicating factors
  • Known pituitary tumors (brain MRI is the study of choice if indicated) or sella CT if MRI is contraindicated or cannot be performed
  • Tumor monitoring in neurocutaneous syndromes as per tumor type‡‡
  • Bone tumor or abnormality of the skull28
  • Histiocytic Neoplasms to assess treatment response and surveillance of known brain/skull lesions29,30
    • Erdheim-Chester Disease
    • Langerhans Cell Histiocytosis
    • Rosai-Dorfman Disease31

Indication for combination studies for the initial pre-therapy staging of cancer, OR active monitoring for recurrence as clinically indicated, OR evaluation of suspected metastases27‡‡

  •  < 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 disorder32,34,35,36

  • New onset of seizures or newly identified change in seizure activity/pattern‡‡ (Brain MRI is the study of choice if indicated.)

For evaluation of known or suspected inflammatory disease or infection (e.g., meningitis or abscess)37,38‡‡

  • Suspected intracranial abscess or brain infection with acute altered mental status OR 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 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‡‡
  • 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-up‡‡39,40
  • 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‡‡41

For evaluation of clinical assessment documenting cognitive impairment of unclear cause42,43,44

  • Change in mental status with a 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)45,46

For evaluation of movement disorders47,48

  • Acute onset of a movement disorder with concern for stroke or hemorrhage‡‡
  • For evaluation of Parkinson’s disease with atypical feature or other movement disorder (i.e., suspected Huntington disease, chorea, parkinsonian syndromes, hemiballismus, atypical dystonia) to exclude an underlying structural lesion‡‡

Note: CT has limited utility in the chronic phases of disease. Brain MRI is the study of choice if indicated. Imaging is not indicated in essential tremor, Tourette’ syndrome or isolated focal dystonia (e.g., blepharospasm, cervical dystonia, laryngeal dystonia, oromandibular dystonia, writer’s dystonia).49,50,51

For evaluation of cranial nerve and visual abnormalities (Brain MRI is the study of choice if indicated.)

  • Abnormal eye findings on physical or neurologic examination (papilledema, nystagmus, ocular nerve palsies, new onset anisocoria, visual field deficit, etc.)52‡‡
  • Note: See background
  • Binocular diplopia with concern for intracranial pathology53 after comprehensive eye evaluation‡‡
  • Childhood strabismus with development delay or abnormal fundoscopic exam to rule out intracranial abnormalities54,55‡‡
  • Horner’s syndrome with symptoms localizing the lesion to the central nervous system56‡‡
  • Evaluation of cranial nerve palsy/neuropathy/neuralgia when thought to be due to tumor, stroke, or bony abnormalities of the skull base or when MRI is contraindicated or cannot be performed57
  • 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 reflex58‡‡
  • 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 jerk59‡‡

For evaluation of known or suspected congenital abnormality (such as craniosynostosis, neural tube defects)60-62

  • 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,63 signs of increased ICP or closed anterior fontanelle‡‡
  • Microcephaly in an infant/child < 18‡‡
  • Craniosynostosis and other head deformities
  • Evaluation of the corticomedullary junction in Achondroplasia64,65‡‡
  • 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 disorder66,67
  • Prior treatment or planned treatment 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/symptoms68,69
  • Initial evaluation for a known syrinx or syringomyelia‡‡
  • Known or suspected normal pressure hydrocephalus (NPH)70
    • With symptoms of gait difficulty, cognitive disturbance, and urinary incontinence
  • Follow-up shunt evaluation71,72,73
    • Post operativity if indicated based on underlying disease and 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) leakage74
  • Cisternography for intermittent and complex CSF rhinorrhea/otorrhea. CSF fluid should always be confirmed with laboratory testing (Beta-2 transferrin assay)75,76
  • Suspected spontaneous intra-cranial hypotension with distinct postural headache other symptoms include: nausea, vomiting, dizziness, tinnitus, diplopia neck pain or imbalance77‡‡
  • †Often congenital, but can present later in life; or less commonly acquired secondary to tumor, stroke, trauma, infection, etc.78

Further evaluation of indeterminate or questionable findings on prior imaging:

  • 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)

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.

Other Indications19,79,80,81

  • Vertigo associated with any of the following:‡‡
    • Signs or symptoms suggestive of a CNS lesion (ataxia, visual loss, double vision, weakness or a change in sensation)82,83
    • 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 year84
    • 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 exam85
  • Syncope with clinical concern for seizure or associated neurological signs or symptoms86,87,88‡‡
  • Cyclical vomiting syndrome or abdominal migraine with any localizing neurological symptoms89,90,91‡‡
  • Soft tissue mass of the head with nondiagnostic initial evaluation (ultrasound and/or radiograph)92,93,94‡‡
  • Psychological changes with neurological deficits on exam or after completion of a full neurological assessment that suggests a possible neurologic cause95‡‡
  • Global developmental delay or developmental delay with abnormal neurological examination in a child < 18 years96,97‡‡
  • Unexplained event (BRUE) formerly apparent life-threatening event (ALTE) in infants < 1 year with concern for neurological cause based on history and exam98‡‡

Note: Imaging is not indicated in low-risk patients

  • Prior to lumbar puncture in patients with suspected increased intracranial pressure or at risk for herniation

Indications for Combination Studies13,14

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: 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 pathology99

  • Brain CT/Neck CTA
    • Recent ischemic stroke or transient ischemic attack
    • Suspected carotid or vertebral artery dissection with focal or lateralizing neurological deficits
  • Brain CT/Brain CTA
    • Recent ischemic stroke or transient ischemic attack
    • 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‡‡
    • Suspected venous thrombosis (dural sinus thrombosis) – Brain CTV (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 > 200‡‡19
  • Brain CT/Brain CTA/Neck CTA
    • Recent stroke or transient ischemic attack (TIA)
    • Suspected carotid or vertebral artery dissection with focal or lateralizing neurological deficits

*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 CT/Orbit CT
    • 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 disorders100‡‡
    • Bilateral optic disk swelling (papilledema) with visual loss101‡‡
  • Brain CT/Cervical CT/Thoracic CT/Lumbar CT (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/symptoms68,69
    • Oncological Applications (e.g., primary nervous system, metastatic)
      • Drop metastasis from brain or spine (CT spine imaging in this scenario is usually CT myelogram) see background
      • Suspected leptomeningeal carcinomatosis (see background)102
      • Tumor evaluation and monitoring in neurocutaneous syndromes
  • 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 - CT spine imaging in this scenario is usually CT myelogram)103

References 

  1. American College of Radiology. ACR Appropriateness Criteria® Headache. American College of Radiology. Updated 2022. Accessed January 23, 2023. https://acsearch.acr.org/docs/69482/Narrative/
  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. 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
  10. 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
  11. 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
  12. Wippold FJ, 2nd. Focal neurologic deficit. AJNR Am J Neuroradiol. Nov 2008;29(10):1998-2000.
  13. American College of Radiology. ACR Appropriateness Criteria®Cerebrovascular Disease-Child. American College of Radiology (ACR). Updated 2019. Accessed January 23, 2023. https://acsearch.acr.org/docs/3102253/Narrative/
  14. American College of Radiology. ACR Appropriateness Criteria®Cerebrovascular Disease. American College of Radiology (ACR). Updated 2016. Accessed January 22, 2023. https://acsearch.acr.org/docs/69478/Narrative/
  15. 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
  16. 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
  17. Arkuszewski M, Melhem ER, Krejza J. Neuroimaging in assessment of risk of stroke in children with sickle cell disease. Adv Med Sci. 2010;55(2):115-29. doi:10.2478/v10039-010-0045-0
  1. 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
  2. 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
  3. American College of Radiology. ACR Appropriateness Criteria® Head Trauma. American College of Radiology (ACR). Updated 2020. Accessed January 23, 2023. https://acsearch.acr.org/docs/69481/Narrative/
  4. Alrajhi KN, Perry JJ, Forster AJ. Intracranial bleeds after minor and minimal head injury in patients on warfarin. J Emerg Med. Feb 2015;48(2):137-42. doi:10.1016/j.jemermed.2014.08.016
  5. 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
  6. Menditto VG, Lucci M, Polonara S, Pomponio G, Gabrielli A. Management of minor head injury in patients receiving oral anticoagulant therapy: a prospective study of a 24-hour observation protocol. Ann Emerg Med. Jun 2012;59(6):451-5. doi:10.1016/j.annemergmed.2011.12.003
  7. 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
  8. American College of Radiology. ACR Appropriateness Criteria® Neuroendocrine Imaging. American College of Radiology. Updated 2018. Accessed January 23, 2023. https://acsearch.acr.org/docs/69485/Narrative/
  9. 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
  10. 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. https://www.nccn.org/professionals/physician_gls/pdf/cns.pdf
  11. Gomez CK, Schiffman SR, Bhatt AA. Radiological review of skull lesions. Insights Imaging. Oct 2018;9(5):857-882. doi:10.1007/s13244-018-0643-0
  12. 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
  13. 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
  14. 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
  15. 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
  16. 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.
  1. 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
  2. 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
  3. American College of Radiology. ACR Appropriateness Criteria®Seizures and Epilepsy. American College of Radiology. May 12, 2023. Updated 2019. Accessed April 27, 2023. https://acsearch.acr.org/docs/69479/Narrative/
  4. 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
  5. Tunkel AR, Glaser CA, Bloch KC, et al. The management of encephalitis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. Aug 1 2008;47(3):303-27. doi:10.1086/589747
  6. Godasi R, Pang G, Chauhan S, Bollu PC. Primary Central Nervous System Vasculitis. StatPearls Publishing. Updated October 12, 2022. Accessed January 23, 2023. https://www.ncbi.nlm.nih.gov/books/NBK482476/
  7. 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.
  8. Graham CB, 3rd, Wippold FJ, 2nd, Pilgram TK, Fisher EJ, Smoker WR. Screening CT of the brain determined by CD4 count in HIV-positive patients presenting with headache. AJNR Am J Neuroradiol. Mar 2000;21(3):451-4.
  9. Harvey PD. Clinical applications of neuropsychological assessment. Dialogues Clin Neurosci. Mar 2012;14(1):91-9. doi:10.31887/DCNS.2012.14.1/pharvey
  10. 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.
  11. 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
  12. 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
  13. McDougall GJ. A review of screening instruments for assessing cognition and mental status in older adults. Nurse Pract. Nov 1990;15(11):18-28.
  14. 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
  15. American College of Radiology. ACR Appropriateness Criteria® Movement Disorders and Neurodegenerative Diseases. American College of Radiology. May 12, 2023. Updated 2019. Accessed April 27, 2023. https://acsearch.acr.org/docs/3111293/Narrative/
  16. 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.
  17. Comella CL, National Organization for Rare Disorders. Cervical Dystonia. National Organization for Rare Disorders (NORD). Updated 2019. Accessed January 23, 2023. https://rarediseases.org/rare-diseases/cervical-dystonia/
  18. 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
  19. 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
  20. 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
  21. Kadom N. Pediatric strabismus imaging. Curr Opin Ophthalmol. Sep 2008;19(5):371-8. doi:10.1097/ICU.0b013e328309f165
  22. 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
  23. 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
  24. American College of Radiology. ACR Appropriateness Criteria® Cranial Neuropathy. American College of Radiology (ACR). Updated 2022. Accessed January 22, 2023. https://acsearch.acr.org/docs/69509/Narrative/
  25. 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
  26. 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
  27. 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
  28. Marchese RF, Schwartz ES, Heuer GG, et al. Reduced Radiation in Children Presenting to the ED With Suspected Ventricular Shunt Complication. Pediatrics. May 2017;139(5)doi:10.1542/peds.2016-2431
  29. Vinocur DN, Medina LS. Imaging in the evaluation of children with suspected craniosynostosis. Evidence-based imaging in pediatrics. Springer; 2010:43-52.
  30. 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
  31. 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
  32. 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
  33. 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
  34. Cerebral palsy in under 25s: assessment and management National Institute for Health and Care Excellence (NICE). Updated January 25, 2017. Accessed January 23, 2023. https://www.nice.org.uk/guidance/ng62/resources/cerebral-palsy-in-under-25s-assessment-and-management-1837570402501
  35. Radic JAE, Cochrane DD. Choosing Wisely Canada: Pediatric Neurosurgery Recommendations. Paediatr Child Health. Sep 2018;23(6):383-387. doi:10.1093/pch/pxy012
  36. 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
  37. Damasceno BP. Neuroimaging in normal pressure hydrocephalus. Dement Neuropsychol. Oct-Dec 2015;9(4):350-355. doi:10.1590/1980-57642015dn94000350
  38. 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
  39. 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
  40. 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
  41. Severson M, Strecker-McGraw MK. Cerebrospinal Fluid Leak. StatPearls Publishing. Updated August 8, 2022. Accessed January 23, 2023. https://www.ncbi.nlm.nih.gov/books/NBK538157/
  42. 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
  43. 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
  44. Gordon N. Spontaneous intracranial hypotension. Dev Med Child Neurol. Dec 2009;51(12):932-5. doi:10.1111/j.1469-8749.2009.03514.x
  45. National Organization for Rare Disorders. Chiari Malformations. National Organization for Rare Disorders (NORD). Updated 2014. Accessed January 23, 2023. https://rarediseases.org/rare-diseases/chiari-malformations/
  46. De Foer B, Vercruysse JP, Pilet B, et al. Single-shot, turbo spin-echo, diffusion-weighted imaging versus spin-echo-planar, diffusion-weighted imaging in the detection of acquired middle ear cholesteatoma. AJNR Am J Neuroradiol. Aug 2006;27(7):1480-2.
  47. 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
  48. Tarrant A, Garel C, Germanaud D, et al. Microcephaly: a radiological review. Pediatr Radiol. Aug 2009;39(8):772-80; quiz 888-9. doi:10.1007/s00247-009-1266-x
  49. 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
  50. 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
  51. 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
  52. Malhotra A, Owens RL. What is central sleep apnea? Respir Care. Sep 2010;55(9):1168-78.
  53. Al-Nsoor NM, Mhearat AS. Brain computed tomography in patients with syncope. Neurosciences (Riyadh). Apr 2010;15(2):105-9.
  54. 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
  55. American College of Physicians. Five things physicians and patients should question: In the evaluation of simple syncope and a normal neurological examination, don’t obtain brain imaging studies (CT or MRI). Choosing Wisely Initiative ABIM Foundation. Updated 2019. Accessed January 23, 2023. https://www.choosingwisely.org/clinician-lists/american-college-physicians-brain-imaging-to-evaluate-simple-syncope/
  56. Angus-Leppan H, Saatci D, Sutcliffe A, Guiloff RJ. Abdominal migraine. Bmj. Feb 19 2018;360:k179. doi:10.1136/bmj.k179
  57. 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
  58. 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
  59. American College of Radiology. ACR Appropriateness Criteria® Soft-Tissue Masses. American College of Radiology. Updated 2022. Accessed January 23, 2023. https://acsearch.acr.org/docs/69434/Narrative/
  60. 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.
  61. 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
  62. 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. https://acsearch.acr.org/docs/3102409/Narrative/
  63. 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
  64. 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.
  1. 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
  2. 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
  3. Behbehani R. Clinical approach to optic neuropathies. Clin Ophthalmol. Sep 2007;1(3):233-46.
  4. 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
  5. Shah LM, Salzman KL. Imaging of spinal metastatic disease. Int J Surg Oncol. 2011;2011:769753. doi:10.1155/2011/769753
  6. Starling A, Hernandez F, Hoxworth JM, et al. Sensitivity of MRI of the spine compared with CT myelography in orthostatic headache with CSF leak. Neurology. Nov 12 2013;81(20):1789-92. doi:10.1212/01.wnl.0000435555.13695.22
  7. 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
  8. 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
  9. Tyagi A. New daily persistent headache. Ann Indian Acad Neurol. Aug 2012;15(Suppl 1):S62-5. doi:10.4103/0972-2327.100011
  10. 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
  11. 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
  12. 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
  13. 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
  14. 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
  15. 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
  16. 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
  17. Coutinho JM. Cerebral venous thrombosis. J Thromb Haemost. Jun 2015;13 Suppl 1:S238-44. doi:10.1111/jth.12945
  18. 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
  19. 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
  20. 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
  21. 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
  22. 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
  23. 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
  24. 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
  25. Ahmed A. MRI features of disseminated 'drop metastases'. S Afr Med J. Jul 2008;98(7):522-3.

Coding Section 

Code Number Description
CPT 70450 Computed tomography, head or brain; without contrast material
  70460 Computed tomography, head or brain; with contrast material(s)
  70470 Computed tomography, head or brain; without contrast material, followed by contrast material(s) and further sections

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" 

History From 2019 Forward     

11/13/2023 Annual review, adding language regarding indeterminate imaging, lesions with atypical features, syrin.syringomalia bulbar and psedobulbar symptoms, abnormal reflexes, new onset headache, tumor surveillance and headache associated with exercise, exertion, Valsalva or sexual activity. Deleting language regarding anosmia or dysomia that is persistent. Entire policy is updated for consistency.
11/29/2022 Annual review, multiple updates to policy including histiocytic neoplasms, pituitary turmors, Arnold Chiarimalformation, cerebral palsy. Verbiage regarding combination studies also updated.

11/08/2021 

Annual review, adding multiple new medical necessity statements related to headaches, langerhans cell histiocytosis, carotid vertebral artery dissection, cisternogrphys and ophthalmalogic issues. Also updating description and references. 

11/01/2020 

Annual review, updating policy for clarification. Also adding additional criteria related to headache, stroke, visual changes. Also updating background and references. 

11/26/2019

New Policy

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