Neurology

Idiopathic Intracranial Hypertension

NOTE: This pathway is intended for use in patients presenting with headache where there is clinical suspicion for idiopathic intracranial hypertension (IIH). IIH is a disorder related to increased intracranial pressure of unknown cause, primarily affecting women of childbearing age (20–50) with a body max index >30.

Last updated: 8/27/2026

Migraine Headache with Worsening

NOTE: This pathway is intended for use in patients with an established history of episodic or chronic migraine presenting with a significant worsening in headache. When approaching a patient with a known history of migraine headache who experiences recent headache worsening, evaluate for recent medication changes and lifestyle factors and determine whether there is a change in headache characteristics or pattern that warrants additional work-up.

Last updated: 8/27/2026

New Onset Headache

NOTE: This pathway is intended for use in patients presenting with new headache and no prior headache history. The majority of individuals presenting with a new headache will likely be diagnosed with a benign headache, however, in a minority a potentially serious etiology may be identified. A systematic approach to headache history and knowledge of the signs and symptoms suggestive of a secondary cause for headache is essential.

Last updated: 8/27/2026

Peripartum Headache

NOTE: This pathway is intended for use in patients who are currently or recently pregnant who experience new or significant worsening of headache. Headache before, during, and after pregnancy are common and typically benign, however, pregnancy-related physiologic changes increase the risk for a secondary cause of headache. Detailed history screening for red flag features is essential, especially when a patient experiences a new headache or a shift in their usual headache pattern.

Last updated: 8/27/2026

Movement Disorders

New onset involuntary movements

NOTE: This pathway is intended for use in patients experiencing new involuntary movements of unclear etiology. History taking should include characterization of the movement(s) phenomenology, including distribution, rhythmicity, onset, progression, exacerbating or alleviating factors, and neurologic symptoms or conditions. History should be obtained from the patient, medical providers, nursing staff, and collateral sources in close contact with the patient when available. An important distinction is whether the abnormal movements: (1) were present prior to hospitalization, (2) were part of the presenting complaint, or (3) developed during hospitalization. Abnormal movements present prior to the hospitalization may suggest a previously undiagnosed movement disorder or neurologic condition. In contrast, Aabnormal movements that develop during the hospitalization are most commonly due to metabolic derangements, toxic exposures, medication related effects, or acute neurologic injury.

Last updated: 8/27/2026

Movement Disorders

Parkinsonism

NOTE: This pathway is intended for use in patients where there is a clinical suspicion for parkinsonism. Parkinsonism is deﬁned as bradykinesia in combination with either rest tremor, rigidity, or both. Parkinson’s Disease is the most common cause of parkinsonism and remains a clinical diagnosis that relies on history and supportive exam findings. Additional etiologies of parkinsonism include drug and toxin-induced, vascular, and other neurodegenerative conditions. A diagnosis of Parkinson’s Disease requires at least 2 cardinal motor manifestations and exclusion of other etiologies.

Last updated: 8/27/2026

Neuro-inflammatory

MS Relapse

NOTE: This pathway should be utilized in patients with an established diagnosis of multiple sclerosis (MS). When evaluating patients with established MS with neurologic symptoms, it is key to identify new symptoms versus worsening of existing symptoms, duration of symptoms, and common precipitating factors. MS is a demyelinating disease process. An MS relapse will have corresponding enhancing lesions on MRI. A pseudo-relapse will not show any new lesions on MRI. If it is a pseudo-relapse, treat the underlying cause (e.g. infection). If it is an MS relapse, treat with steroids, and if severe, IVIG/PLEX. Other demylinating diseases to keep on your differential are NMO, MOG, CNS Sjogren's, and toxic, inflammatory and metabolic disorders.

Last updated: 8/28/2026

Neuro-inflammatory

Optic Neuritis

NOTE: This pathway is intended for use in patients where there is a high clinical suspicion for vision symptoms to be secondary to optic nerve dysfunction resulting in optic neuritis/neuropathy. Questions are designed to help differentiate between the different etiologies for this. Inflammation of the optic nerve is a commonly associated with multiple sclerosis (as a presenting symptom or during the course of the disease), however, many other conditions may cause optic nerve dysfunction which can often be elicited through a comprehensive history.

Last updated: 8/28/2026

Neuromuscular

Inability to Wean from Ventilator

NOTE: This pathway is intended for use in patients in the intensive care unit who are unable to be extubated due to a suspected neurologic cause. Neuromuscular cause for respiratory weakness should be considered in a patient whose mental status does not preclude extubation and other contributing conditions (pulmonary, cardiac, etc.) have been excluded. Diaphragmatic weakness resulting in the inability to wean a patient from mechanical ventilation may be due to a previously undiagnosed or subclinical neuromuscular condition or due to hospitalization or iatrogenic causes, with ICU acquired diaphragmatic weakness remaining a common etiology in the in-patient setting. History taking should include inquiring about symptoms of neuromuscular weakness prior to hospitalization to suggest a primary neurologic cause. History from the patient is often limited given the patient’s intubated state and therefore obtaining collateral history from individuals in close contact with the patient is crucial.

Last updated: 8/27/2026

Myasthenia Gravis (Post-Operative Assessment)

NOTE: This pathway is intended for use in patients with an established diagnosis of myasthenia gravis who have undergone an in-patient procedure or surgery. Worsening of symptoms of myasthenia gravis Is a known potential complication following surgery. History should focus on understanding baseline deficits (if present) and identifying new or worsening post-op deficits, in conjunction with the neurologic exam and ancillary studies such as respiratory parameters.

Last updated: 8/27/2026

Myasthenia Gravis (suspected or established diagnosis)

NOTE: This pathway is intended for use in patients where there is a high clinical suspicion for a new diagnosis of myasthenia gravis based on signs and symptoms OR for patients with an established diagnosis of myasthenia gravis and concern for disease worsening. Myasthenia gravis is a chronic autoimmune neuromuscular disorder with a bimodal age distribution classified as early onset (age 20s-30s, women > men and late-onset (age 60s-80s men > female). Symptoms may seem relatively non-specific. A history of fatiguing/fluctuating weakness involving preferentially affected muscle groups adds to diagnostic certainty.

Last updated: 8/27/2026

New onset weakness

NOTE: This pathway should be utilized in patients presenting with acute onset and/or rapidly progressive weakness. History taking should focus on identifying the extent of weakness, presence or absence of other neurologic symptoms, temporal progression of symptoms, identification of antecedent triggers, and associated conditions. Weakness secondary to primary brain conditions are not included in this template.

Last updated: 8/27/2026

Peripheral facial weakness

NOTE: This pathway is intended for use in patients presenting with a peripheral pattern of facial weakness and questions are designed to help differentiate between the different etiologies. Peripheral (lower motor neuron) facial weakness is characterized by weakness involving both the upper and lower portion of the face. This presentation localizes most commonly to the facial nerve and its branches and less commonly within the facial nucleus (within the lower portion of the dorsolateral pons), or within the subarachnoid space (within the cerebellopontine cistern). The most common cause of lower motor neuron pattern of facial weakness is Bell’s Palsy, which typically involves one side of the face and is associated with reactivation of latent herpes viruses. Many other etiologies for facial weakness exist and can be differentiated based on associated symptoms, medical history, pattern of weakness (ipsilateral versus bilateral) and other associated exam findings.

Last updated: 8/27/2026

Seizure/Syncope/Dizziness

Acute Onset Dizziness

NOTE: This pathway is intended for use in patients presenting with symptoms of acute onset dizziness. Utilizing a timing and triggers approach to acute onset dizziness often identifies an underlying etiology for the patient’s presentation.

Last updated: 8/27/2026

Breakthrough Seizure

NOTE: This pathway is intended for use in patients who have an established diagnosis of epilepsy and present with breakthrough seizure(s). Breakthrough seizures in patients with known epilepsy are most commonly due to medication nonadherence, metabolic disturbances, infection, sleep deprivation, or medication interactions. Evaluation focuses on identifying the precipitating factor and correcting it.

Last updated: 8/27/2026

First Time Seizure in an Adult

NOTE: This pathway is intended for the clinical scenario where the clinical suspicion for seizure is relatively high. If there is uncertainty regarding the episode(s) in question consider utilizing the seizure versus syncope pathway. Evaluation of a first-time seizure-like event begins with careful characterization of the event. Many paroxysmal events that appear to be seizures are actually convulsive syncope, psychogenic events, or other non-epileptic conditions. The goal of the history is to determine whether the event was truly epileptic, identify possible provoking factors, and guide the initial diagnostic workup.

Last updated: 8/27/2026

Orthostatic Hypotension/Autonomic Dysfunction

NOTE: This pathway is intended for use in patients presenting with clinical evidence of orthostatic hypotension and/or autonomic dysfunction of unclear etiology. Orthostatic hypotension (OH) is defined as a fall in blood pressure (>20 mm Hg fall in systolic BP OR >10 mm Hg fall in diastolic BP) that occurs within three minutes of standing up from a lying or seated position. Through history taking and vitals assessment, OH should be classified as neurogenic and/or non-neurogenic, with specific etiologies identified. Neurogenic orthostatic hypotension is caused by dysfunction of the baroreceptor reflex. Non-neurogenic causes for orthostatic hypotension are more common and are a result of external reversible factors that impair normal hemodynamic compensation.

Last updated: 8/27/2026

Seizure Versus Syncope

NOTE: This pathway is intended for use in patients who experienced a paroxysmal episode of loss of consciousness or alteration of awareness. If clinical suspicion for seizure is high, consider utilizing first time seizure pathway. It can be difficult to differentiate seizures from syncope, but directed questions involving the semiology of the episode and associated symptoms can help differentiate the two.

Last updated: 8/27/2026