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 aura^6,7,107— 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 carcinomatosis^{118,119,120,121} — 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
Headache
Evaluation of Headache

• Chronic headache with a change in character/pattern (e.g., more frequent, increased severity, or duration) ⁽¹⁾ 
• 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 causes ^(1,2)
• 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 (Sudden onset new headache reaching maximum intensity within 2-3 minutes, lasting more than 5 minutes).
  • Prior history of stroke or intracranial bleed
  • Known coagulopathy or on anticoagulation
• New onset of headache with any of the following ^(1,3,4):
  • 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 ^(1,3)
  • 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 worsening ^(1,5,6,7) 
  • Persistent or progressively worsening during a course of physician-directed treatment ⁽¹⁾ 

Note: Neuroimaging warranted for atypical/complex migraine aura, but not for a typical migraine aura (1) (see background)

Special Considerations in the Pediatric Population with Persistent Headache (8,9)

• 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)

Neurological Symptoms or Deficits
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).

Stroke and Vascular Disease
Evaluation of Known or Suspected Stroke (15,16)

• 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 neurological signs or symptoms in sickle cell disease ^(17,18)
• High stroke risk in sickle cell patients (2 - 16 years of age) with a transcranial doppler velocity >200 ⁽¹⁹⁾ 

Evaluation of Known or Suspected Vascular Disease

• Known Moyamoya disease or reversible cerebral vasoconstriction with any new or changing neurological signs or symptoms
• Follow-up for known hemorrhage, hematoma, or vascular abnormalities

Head Trauma
Evaluation of Known or Suspected Trauma (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 

Brain Tumor, Mass, or Metastasis
Evaluation of Suspected Tumor/Mass/Cyst (1,25)

• Erdheim-Chester Disease
• Langerhans Cell Histiocytosis
• Rosai-Dorfman Disease

Note: Suspected Pituitary Tumors (Brain MRI is the study of choice if indicated) or Sella CT if MRI is contraindicated or cannot be performed
Note: Screening for hereditary cancers syndromes (Brain MRI is the study of choice if indicated)

Evaluation of Known Brain Lesion/Cyst

• Bone tumor or abnormality of the skull ⁽²⁶⁾
• Histiocytic Neoplasms to assess treatment response and surveillance of known brain/skull lesions ^(27,28)
  • Erdheim-Chester Disease
  • Langerhans Cell Histiocytosis
  • Rosai-Dorfman Disease

Note: Known pituitary tumors (Brain MRI is the study of choice if indicated) or Sella CT if MRI is contraindicated or cannot be performed

CT for Known Cancer
MRI is the ideal modality to follow-up meningioma, pituitary tumors, low grade tumors, neurocutaneous syndromes, and screening/restaging/surveillance for non-CNS cancers. CT should only be used when MRI is contraindicated or is unable to be obtained.
MRI is appropriate for any malignancy when there are signs or symptoms of brain metastases (e.g., headache, sensory deficits, memory problems). There does not need to be a neuro deficit on exam or other workup done first for a patient with cancer.

Combination Studies for Initial Staging, Active Monitoring, or Evaluation of Suspected Metastases (25)
< 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

Seizure Disorders
For Evaluation of Known or Suspected Seizure Disorder (29,30,31)

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

Infectious or Inflammatory Disease
Evaluation of Known or Suspected Infection or Inflammatory Disease 

• 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) ⁽³²⁾
• 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 ⁽³³⁾
• 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

Cognitive Impairment
Evaluation of Cognitive Impairment (34,35)

• 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) ^(36,37)

Movement Disorders
Evaluation of Movement Disorders (11,38)

• For evaluation of acute onset of a movement disorder with concern for stroke or hemorrhage
• For evaluation of suspected Parkinson’s with atypical feature or unresponsive to levodopa
• Note: Atypical parkinsonian syndromes include progressive supranuclear palsy (PSP), multiple system atrophy (MSA), corticobasal degeneration (CBD), and dementia with Lewy bodies.
• For the evaluation of other movement disorder to exclude a structural lesion (i.e., suspected Huntington disease, chorea, hemiballismus, atypical dystonia)

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) (38,39).

Cranial Nerve and Vision Abnormalities
Vision Abnormalities 

• Abnormal eye findings on physical or neurologic examination (papilledema, pathologic nystagmus, optic atrophy, ocular nerve palsies, new onset anisocoria, visual field deficit, etc.) Note: See background
• Binocular diplopia with concern for intracranial pathology after comprehensive eye evaluation ⁽⁴⁰⁾
• Childhood strabismus with development delay or abnormal fundoscopic exam to rule out intracranial abnormalities ⁽⁴¹⁾
• Horner’s syndrome with symptoms localizing the lesion to the central nervous system (42)

Other Cranial Neuropathies

• 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 jerk ⁽⁴⁴⁾ 

Congenital Abnormalities
Evaluation of Known or Suspected Congenital Abnormalities

• 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 fontanelle ⁽⁴⁵⁾ 
• Evaluation of microcephaly in an infant/child < 18 ⁽⁴⁶⁾ 
• Evaluation of craniosynostosis and other skull deformities. ^(47,48)
• Evaluation of the corticomedullary junction in Achondroplasia ⁽⁴⁹⁾ 
• 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 disorder ⁽⁵⁰⁾
• Prior treatment OR treatment planned for congenital abnormality

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

Cerebrospinal Fluid Abnormalities
Evaluation of Known or Suspected CSF Abnormalities