Neurology

01 Neuroanatomy & Neurophysiology Essentials

Neurology is the medical (non-surgical) specialty managing disorders of the brain, spinal cord, peripheral nerves, neuromuscular junction, and muscle. A strong scribe understands the anatomic substrate for every complaint because neurologists localize before they diagnose — the single most important question in a neurology note is "where is the lesion?"

The Central Nervous System

The cerebrum is divided into two hemispheres joined by the corpus callosum. Each hemisphere has four lobes: the frontal (executive function, motor planning, Broca's speech area on the dominant side, personality), parietal (primary somatosensory cortex, spatial processing, the dominant-hemisphere angular gyrus for reading/writing), temporal (hearing, memory via hippocampus, Wernicke's receptive language area on the dominant side), and occipital (primary visual cortex). The diencephalon contains the thalamus (sensory relay) and hypothalamus (autonomic/endocrine). The basal ganglia (caudate, putamen, globus pallidus, substantia nigra, subthalamic nucleus) orchestrate movement. The cerebellum coordinates smooth movement, balance, and gait. The brainstem — midbrain, pons, medulla — houses the cranial nerve nuclei, reticular activating system, and long tracts.

Vascular Supply

The brain is perfused by the anterior circulation (internal carotid → anterior and middle cerebral arteries) and the posterior circulation (vertebral arteries → basilar artery → posterior cerebral arteries, plus PICA, AICA, SCA to the cerebellum/brainstem). These connect at the circle of Willis via the anterior and posterior communicating arteries. Stroke syndromes are named for the occluded vessel: an MCA stroke produces contralateral arm-face weakness and, on the dominant side, aphasia; an ACA stroke produces contralateral leg weakness; a PCA stroke produces homonymous hemianopia; lacunar strokes in deep perforators produce pure motor, pure sensory, or ataxic-hemiparesis syndromes without cortical findings.

Cranial Nerves & Tracts

The 12 cranial nerves must be memorized: I olfactory, II optic, III oculomotor, IV trochlear, V trigeminal, VI abducens, VII facial, VIII vestibulocochlear, IX glossopharyngeal, X vagus, XI accessory, XII hypoglossal. The long tracts — corticospinal (motor), dorsal columns (proprioception/vibration), spinothalamic (pain/temperature) — run through the spinal cord with characteristic crossing patterns that let the neurologist localize spinal cord lesions to a specific level and side.

02 Scribe Documentation Framework

Neurology notes are organized around localization and temporal profile. A well-written neurology HPI tells the reader, in order, what happened, when, how fast it came on, what systems are involved, and where in the nervous system the process lives. Neurology encounters fall into three buckets: acute (ED stroke, status epilepticus, ICH), outpatient subspecialty (headache, MS, epilepsy, movement, memory), and consultative (inpatient "altered mental status," "new weakness," "seizure?").

03 Ischemic Stroke & TIA Vascular

Ischemic stroke accounts for roughly 87% of all strokes. It results from occlusion of a cerebral artery, producing focal neurologic deficit from infarction of the territory it supplies. Transient ischemic attack (TIA) is a brief episode of focal neurologic dysfunction from ischemia without infarction on imaging — time-based definitions ("< 24 hours") have been replaced by tissue-based definitions.

Risk Factors & Comorbidities

Subtypes (TOAST Classification)

• Large artery atherosclerosis — carotid or intracranial plaque causing artery-to-artery embolism or hemodynamic failure.
• Cardioembolic — most commonly atrial fibrillation; also LV thrombus, endocarditis, patent foramen ovale with paradoxical embolism.
• Small vessel (lacunar) — lipohyalinosis of deep penetrating arteries. Classic syndromes: pure motor hemiparesis (internal capsule), pure sensory (thalamus), ataxic hemiparesis, dysarthria-clumsy hand.
• Other determined etiology — dissection, vasculitis, hypercoagulable state, sickle cell.
• Cryptogenic / undetermined — workup negative or incomplete. Often pushed toward extended rhythm monitoring to look for occult AFib.

Clinical Presentation by Territory

Acute Management

The first step is NCCT of the head to exclude hemorrhage, followed by CTA head and neck to identify large vessel occlusion (LVO), and often CT perfusion to assess salvageable penumbra. 2019 AHA/ASA Guidelines for the Early Management of Acute Ischemic Stroke are the standard citation. IV thrombolysis with alteplase (tPA) 0.9 mg/kg is indicated within 4.5 hours of LKW in eligible patients; tenecteplase (TNK) 0.25 mg/kg single bolus is now widely used as a more practical alternative and is supported by multiple non-inferiority trials. Mechanical thrombectomy for LVO is standard up to 6 hours and up to 24 hours in selected patients with favorable imaging (DAWN, DEFUSE-3).

Blood pressure is managed with "permissive hypertension" (up to 220/120) in non-thrombolysis patients to maintain perfusion; targets are lowered to <185/110 before tPA and <180/105 for 24 hours after. Secondary prevention starts immediately: antiplatelet (aspirin 81 mg, or clopidogrel; dual antiplatelet with aspirin + clopidogrel for 21–90 days after minor stroke or high-risk TIA per CHANCE and POINT), high-intensity statin, BP control, glycemic control, smoking cessation, and anticoagulation for cardioembolic sources. The 2021 AHA/ASA Guideline for the Prevention of Stroke in Patients with Stroke and TIA is the foundational citation for secondary prevention.

04 Intracerebral Hemorrhage (ICH) Vascular

Spontaneous ICH accounts for ~10–15% of strokes but carries the highest mortality of any stroke subtype — 30-day mortality ~40% and only about 20% of survivors regain functional independence. Etiologies: hypertensive arteriopathy (deep bleeds in basal ganglia, thalamus, pons, cerebellum from lipohyalinosis of perforating arteries), cerebral amyloid angiopathy (CAA) (lobar bleeds and microbleeds in elderly, from amyloid deposition in cortical/leptomeningeal vessels), vascular malformations (AVM, cavernoma, dural AV fistula), coagulopathy/anticoagulation, hemorrhagic conversion of ischemic stroke, tumor hemorrhage (especially melanoma, RCC, thyroid, choriocarcinoma, GBM), venous sinus thrombosis with venous infarct, sympathomimetic drug use (cocaine, methamphetamine), and reversible cerebral vasoconstriction syndrome (RCVS).

Presentation & Workup

Abrupt focal deficit often with headache, vomiting, and depressed level of consciousness — more likely than ischemic stroke to present with reduced GCS and early clinical decline. Deep bleeds produce hemiparesis out of proportion to cortical signs; cerebellar bleeds present with headache, vomiting, ataxia, and risk of brainstem compression; pontine bleeds produce coma, pinpoint pupils, and crossed findings. NCCT shows hyperdense (~60–80 HU) blood immediately and quantifies volume using the ABC/2 formula. CTA identifies a "spot sign" (active contrast extravasation, predicting hematoma expansion) and excludes an underlying vascular lesion. MRI with gradient echo or susceptibility-weighted imaging reveals microbleeds that support a CAA diagnosis (Boston criteria). Labs: CBC with platelets, PT/INR, PTT, anti-Xa, type and screen, basic chemistries, toxicology.

Management

Per 2022 AHA/ASA ICH Guideline: aggressive SBP lowering to ~140 mmHg is reasonable in mild-moderate ICH (INTERACT-2, ATACH-2), reversal of any anticoagulation is mandatory (4-factor PCC for warfarin with vitamin K, idarucizumab for dabigatran, andexanet alfa or 4F-PCC for factor Xa inhibitors, platelets are generally NOT indicated in antiplatelet-associated ICH per PATCH), seizure prophylaxis only if seizures occur or in lobar ICH with depressed consciousness, neurosurgical evacuation for cerebellar hemorrhage > 3 cm or with brainstem compression/hydrocephalus, external ventricular drainage for obstructive hydrocephalus or large IVH, and ICU-level monitoring including head-of-bed elevation, normothermia, and osmotherapy (mannitol, hypertonic saline) for elevated ICP. The ICH Score (0–6) predicts 30-day mortality based on GCS, ICH volume, IVH, infratentorial origin, and age ≥ 80. Minimally invasive surgical evacuation (MISTIE, ENRICH) is an evolving option for selected supratentorial ICH.

05 Subarachnoid Hemorrhage (SAH) Vascular

Non-traumatic SAH is most commonly due to rupture of a saccular (berry) aneurysm at the circle of Willis. The hallmark presentation is the thunderclap headache — "the worst headache of my life," reaching maximum intensity within seconds. Associated features include neck stiffness, photophobia, transient LOC, and vomiting. NCCT within 6 hours is >95% sensitive; if negative but suspicion remains high, lumbar puncture looking for xanthochromia is standard. CTA or catheter angiography identifies the aneurysm.

Grading & Management

Severity is graded by the Hunt and Hess scale (I asymptomatic/mild headache; II moderate-severe headache, nuchal rigidity, no deficit; III drowsy, mild deficit; IV stupor, moderate-severe hemiparesis; V deep coma, decerebrate posturing) and the modified Fisher scale based on CT blood burden. Management per 2023 AHA/ASA Aneurysmal SAH Guideline includes early aneurysm securing (clip or coil within 24–72 hours), nimodipine 60 mg PO q4h for 21 days to reduce delayed cerebral ischemia from vasospasm, BP control, and ICU monitoring with transcranial Doppler for vasospasm surveillance days 4–14.

06 Headache Disorders Medical

Headache is the most common neurology complaint. The scribe must distinguish primary headaches (migraine, tension, cluster) from secondary causes (SAH, meningitis, tumor, IIH, dissection, giant cell arteritis). The red-flag mnemonic SNOOP — Systemic symptoms, Neurologic deficits, Onset thunderclap, Older age new-onset, Pattern change — drives the decision to image.

Migraine

Episodic, recurrent, unilateral (often), pulsating, moderate-to-severe headache lasting 4–72 hours, worsened by activity, with nausea, photophobia, or phonophobia. Migraine with aura includes transient visual (scintillating scotoma, fortification spectra), sensory, or language phenomena lasting 5–60 minutes. Abortive therapy: triptans (sumatriptan 100 mg PO or 6 mg SC, rizatriptan, eletriptan), NSAIDs, gepants (ubrogepant, rimegepant), lasmiditan. Preventive therapy (indicated at ≥4 headache days/month): beta blockers (propranolol, metoprolol), topiramate, valproate, amitriptyline, candesartan, and the CGRP monoclonal antibodies (erenumab, fremanezumab, galcanezumab, eptinezumab). OnabotulinumtoxinA (Botox) every 12 weeks is approved for chronic migraine (≥15 headache days/month). AHS 2021 Consensus Statement on Migraine Prevention is the standard citation.

Tension-Type Headache

Bilateral, pressing/tightening ("band-like"), mild-to-moderate, no nausea, no photo/phonophobia (or one but not both). Managed with NSAIDs, stress reduction, and TCA prophylaxis if frequent.

Cluster Headache

Severe unilateral orbital/periorbital pain in bouts of 15–180 minutes, occurring up to 8 times/day, with ipsilateral autonomic features (conjunctival injection, lacrimation, rhinorrhea, ptosis, miosis) and restlessness. Acute treatment: high-flow O2 12–15 L/min via non-rebreather and SC sumatriptan. Preventive: verapamil, short steroid bridge, galcanezumab.

Secondary Headache — Trigeminal Neuralgia, IIH, GCA

Trigeminal neuralgia: lancinating, electric-shock facial pain in V2/V3 distribution triggered by light touch, chewing, brushing teeth. First-line therapy is carbamazepine or oxcarbazepine; refractory cases go for microvascular decompression or percutaneous rhizotomy. Idiopathic intracranial hypertension (IIH): typically obese young woman with daily headaches, pulsatile tinnitus, transient visual obscurations, and papilledema; LP opening pressure >25 cm H₂O. Treat with weight loss and acetazolamide; VP shunt or optic nerve sheath fenestration for vision-threatening disease. Giant cell arteritis: >50 yo with new temporal headache, jaw claudication, scalp tenderness, PMR, ESR/CRP elevated — start high-dose steroids immediately and biopsy within 1–2 weeks.

07 Seizures & Epilepsy Paroxysmal

A seizure is a transient occurrence of signs/symptoms due to abnormal excessive or synchronous neuronal activity. Epilepsy is defined as ≥2 unprovoked seizures >24 hours apart, or one unprovoked seizure with high recurrence risk. The ILAE classification divides seizures into focal (with or without impaired awareness; with or without motor features), generalized (tonic-clonic, absence, myoclonic, atonic, tonic, clonic), and unknown onset.

Semiology the Scribe Will Hear

Focal aware (formerly "simple partial"): preserved consciousness with a localized sensation — déjà vu, rising epigastric sensation (temporal lobe), unilateral jerking (motor strip). Focal impaired awareness (formerly "complex partial"): blank staring, oral and manual automatisms, postictal confusion. Generalized tonic-clonic: sudden LOC, tonic stiffening, clonic jerking, tongue biting (lateral), incontinence, postictal confusion lasting minutes to an hour.

Workup

MRI brain to look for structural lesion, EEG (routine, prolonged, or inpatient video-EEG) to capture interictal epileptiform discharges or ictal events, labs including glucose, electrolytes, magnesium, toxicology, and LP if CNS infection is suspected.

Status Epilepticus

Defined as a seizure >5 minutes or recurrent seizures without return to baseline. Treatment algorithm per Neurocritical Care Society / AES Guideline: first-line IV lorazepam 4 mg (or IM midazolam 10 mg); second-line loading with IV levetiracetam 60 mg/kg, fosphenytoin 20 mg PE/kg, or valproate 40 mg/kg (ESETT trial showed equivalence); third-line is anesthetic-level sedation with midazolam, propofol, or pentobarbital infusions in the ICU with continuous EEG monitoring.

Chronic Management

Antiseizure medications (ASMs) are chosen by seizure type, comorbidities, pregnancy potential, and side-effect profile. Broad-spectrum agents (effective for focal and generalized): lamotrigine, levetiracetam, valproate, topiramate, zonisamide. Narrow-spectrum (focal only): carbamazepine, oxcarbazepine, phenytoin, lacosamide. Absence seizures respond to ethosuximide or valproate. Valproate is teratogenic and contraindicated in pregnancy whenever possible. Lamotrigine requires slow titration due to Stevens-Johnson risk. AAN Guideline on Treatment of New-Onset Epilepsy is the standard citation.

08 Syncope & Transient Loss of Consciousness Paroxysmal

Neurologists are consulted to distinguish syncope (global cerebral hypoperfusion, brief, rapid return to baseline) from seizure (cortical electrical event, often with postictal state). Cardiogenic syncope (arrhythmia, structural heart disease) is managed by cardiology but overlaps with neurology work-up. Key distinguishing features: tongue biting (lateral → seizure, tip → nonspecific), incontinence (nonspecific), duration of LOC (seconds in syncope vs minutes in seizure), postictal confusion and myalgias (absent in syncope, typical in tonic-clonic), preceding aura or déjà vu (seizure), preceding warmth/nausea/tunnel vision (vasovagal), and position at onset (supine onset favors seizure or arrhythmia). Convulsive syncope — brief myoclonic jerks at the end of a vasovagal episode — is commonly mistaken for seizure but lacks a true postictal state.

Workup: ECG in every patient, orthostatic vitals, echo if structural disease is suspected, and Holter, 30-day event monitor, or implantable loop recorder for recurrent unexplained syncope. Tilt-table testing identifies neurocardiogenic and orthostatic causes. EEG and MRI brain are not routinely indicated in classic vasovagal syncope — they are reserved for cases with features suggestive of seizure or a focal deficit.

09 Multiple Sclerosis & Demyelinating Disease Demyelinating

Multiple sclerosis (MS) is an autoimmune demyelinating disease of the CNS characterized by lesions disseminated in space and time. Onset is typically age 20–40, female predominant. Phenotypes: clinically isolated syndrome (CIS), relapsing-remitting MS (RRMS) (~85% at onset), secondary progressive MS (SPMS), and primary progressive MS (PPMS).

Clinical Presentations

• Optic neuritis — painful unilateral vision loss with afferent pupillary defect and central scotoma, typically recovering over weeks.
• Transverse myelitis — spinal cord syndrome with paraparesis, sensory level, bowel/bladder dysfunction. Lhermitte sign (electric shock with neck flexion).
• Brainstem/cerebellar — internuclear ophthalmoplegia (bilateral INO is essentially pathognomonic in a young adult), vertigo, ataxia.
• Cerebral — cognitive changes, hemisensory or hemimotor symptoms.
• Uhthoff phenomenon — symptom worsening with heat or exercise.

Diagnosis

McDonald criteria require dissemination in space (≥2 typical CNS regions on MRI) and time (simultaneous enhancing and non-enhancing lesions, or new lesions on follow-up MRI). CSF shows oligoclonal bands unique to CSF in ~85% of MS patients. Evoked potentials (visual, somatosensory) may show subclinical demyelination.

Management

Acute relapses: high-dose IV methylprednisolone 1 g daily x 3–5 days (PO equivalents acceptable per AAN evidence review); plasma exchange for steroid-refractory attacks. Disease-modifying therapies (DMTs): injectables (interferon beta-1a/1b, glatiramer acetate), oral agents (dimethyl fumarate, diroximel fumarate, fingolimod and other S1P modulators ozanimod/ponesimod/siponimod, teriflunomide, cladribine), and high-efficacy monoclonals (natalizumab — monitor JC virus for PML risk; ocrelizumab — anti-CD20, approved for RRMS and PPMS; ofatumumab, ublituximab; alemtuzumab). Treatment selection is driven by disease activity, patient preference, pregnancy plans, and safety monitoring needs. AAN 2018 Practice Guideline on DMTs for MS is the standard citation.

NMO and MOGAD

Neuromyelitis optica spectrum disorder (NMOSD) is a distinct astrocytopathy with aquaporin-4 IgG antibodies, classically producing severe optic neuritis and longitudinally extensive transverse myelitis (≥3 vertebral segments). Treated with rituximab, eculizumab, inebilizumab, or satralizumab — NOT standard MS DMTs, which can worsen it. MOGAD (myelin oligodendrocyte glycoprotein antibody disease) overlaps clinically and is managed with immunotherapy.

10 Amyotrophic Lateral Sclerosis Degenerative

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting both upper motor neurons (corticospinal tract — spasticity, hyperreflexia, Babinski, pseudobulbar affect) and lower motor neurons (anterior horn cells — weakness, atrophy, fasciculations, cramps). The hallmark is mixed UMN and LMN findings in the same body segment. Median survival is 3–5 years, most commonly from respiratory failure, though ~10% live longer than 10 years. About 10% of cases are familial (most commonly C9orf72 hexanucleotide expansion, SOD1, FUS, TARDBP mutations). Up to 50% of ALS patients have measurable cognitive or behavioral involvement on the ALS-FTD spectrum.

Clinical Phenotypes & Diagnosis

Presentations include limb-onset (asymmetric foot drop or hand weakness that spreads), bulbar-onset (dysarthria, dysphagia, tongue atrophy and fasciculations, sialorrhea, emotional lability), and respiratory-onset (orthopnea, dyspnea on exertion, morning headache from nocturnal hypoventilation). Progressive muscular atrophy (pure LMN) and primary lateral sclerosis (pure UMN) are related motor neuron disorders on the same continuum. Diagnosis is clinical with EMG confirmation — EMG shows widespread denervation with fasciculations, positive sharp waves, fibrillation potentials, and chronic reinnervation changes (large-amplitude long-duration motor unit potentials). MRI is typically used to exclude mimics such as cervical spondylotic myelopathy, multifocal motor neuropathy with conduction block (responds to IVIG), Kennedy disease, and paraneoplastic motor neuronopathy. Revised El Escorial / Awaji criteria guide diagnostic certainty.

Management

Care is delivered through multidisciplinary ALS clinics combining neurology, pulmonology, PT/OT, speech, nutrition, respiratory therapy, and palliative care. Disease-modifying therapies: riluzole 50 mg BID (glutamate antagonist, modestly prolongs survival ~3 months), edaravone (IV or PO, free-radical scavenger, slows functional decline in selected patients with preserved function), tofersen for SOD1-ALS (antisense oligonucleotide). Symptomatic care includes non-invasive ventilation (BiPAP) when FVC falls below ~50% predicted, PEG feeding when dysphagia and weight loss become unsafe, secretion management (glycopyrrolate, scopolamine, suction), spasticity treatment (baclofen, tizanidine), dextromethorphan/quinidine for pseudobulbar affect, and early hospice/palliative integration. Serial monitoring uses the ALSFRS-R functional scale and pulmonary function tests.

11 Parkinson Disease & Parkinsonism Movement

Parkinson disease (PD) is the second most common neurodegenerative disorder after Alzheimer. Pathology: loss of dopaminergic neurons in the substantia nigra pars compacta with alpha-synuclein-containing Lewy bodies. The MDS Clinical Diagnostic Criteria (Postuma et al., 2015) require bradykinesia plus rest tremor and/or rigidity, with supportive features and absence of absolute exclusion criteria.

Cardinal Features — "TRAP"

• Tremor at rest, 4–6 Hz, pill-rolling, asymmetric onset.
• Rigidity — lead-pipe or cogwheel.
• Akinesia/bradykinesia — slowness, hypomimia, micrographia, decreased arm swing.
• Postural instability (later feature) — positive pull test, retropulsion, falls.

Non-motor features are now recognized as major drivers of disability: REM sleep behavior disorder (often premotor), hyposmia, constipation, orthostatic hypotension, urinary urgency, depression, anxiety, and cognitive impairment/PDD in later disease. Severity is staged with Hoehn & Yahr (I unilateral; II bilateral no balance impairment; III mild bilateral with postural instability, physically independent; IV severe disability, still able to walk/stand unassisted; V wheelchair/bedbound) and functional impact with MDS-UPDRS.

Atypical Parkinsonism ("Parkinson-Plus")

Treatment

First-line for motor symptoms is carbidopa/levodopa, the most effective dopaminergic therapy. Dopamine agonists (pramipexole, ropinirole, rotigotine patch) are often used in younger patients to delay levodopa-induced dyskinesia but carry impulse-control disorder risk. MAO-B inhibitors (selegiline, rasagiline, safinamide) and COMT inhibitors (entacapone, opicapone) extend levodopa action. Amantadine reduces dyskinesia. Advanced therapies include deep brain stimulation (DBS) of the STN or GPi, continuous subcutaneous apomorphine, and levodopa-carbidopa intestinal gel (Duopa).

12 Other Movement Disorders Movement

Essential tremor (ET) is the most common movement disorder: bilateral, largely symmetric postural and kinetic hand tremor (worse with target-directed activity such as pouring or drinking from a cup), often with head ("no-no" or "yes-yes") and voice involvement, frequently familial (autosomal dominant in many pedigrees), classically improved by small amounts of alcohol, worsened by caffeine, fatigue, and stress. Distinguishing ET from PD hinges on tremor phenomenology (action in ET vs rest in PD), absence of bradykinesia and rigidity, symmetry, and DaTscan normality if needed. Treatment: first-line propranolol 60–320 mg/day or primidone titrated up to 250–750 mg/day; second-line topiramate, gabapentin, or benzodiazepines; refractory cases are excellent candidates for DBS of the ventral intermediate nucleus (VIM) of the thalamus or MR-guided focused ultrasound thalamotomy.

Huntington disease (HD) is an autosomal dominant CAG trinucleotide repeat expansion in the HTT gene on chromosome 4, with anticipation (earlier onset in successive generations, especially paternal inheritance). Typical age of onset 30–50. The classic triad is chorea (involuntary dance-like movements), psychiatric symptoms (depression, irritability, psychosis, suicidality), and progressive cognitive decline/dementia. Atrophy of the caudate nucleus produces the "boxcar" appearance on imaging. Genetic testing confirms diagnosis and guides family counseling. Symptomatic treatment: tetrabenazine, deutetrabenazine, or valbenazine (VMAT2 inhibitors) suppress chorea; SSRIs and atypical antipsychotics for mood and psychosis. No disease-modifying therapy is yet available.

Wilson disease is an autosomal recessive copper-transport disorder (ATP7B gene) presenting in adolescents and young adults with tremor (classically "wing-beating"), dystonia, parkinsonism, cerebellar signs, psychiatric symptoms, liver disease, and Kayser-Fleischer rings on slit-lamp exam. Screen with low serum ceruloplasmin, elevated 24-hour urinary copper, and slit-lamp exam; liver biopsy and genetic testing confirm. Treat with copper chelation (penicillamine, trientine) and zinc (which blocks intestinal copper absorption). Life-long therapy is required.

Dystonia is sustained or intermittent muscle contractions causing twisting, repetitive movements, or abnormal postures. It can be focal (cervical dystonia/spasmodic torticollis, blepharospasm, oromandibular dystonia, writer's cramp, laryngeal dystonia/spasmodic dysphonia), segmental, multifocal, or generalized (often genetic, including DYT1). Secondary dystonia can result from dopamine-blocking medications (tardive), stroke, or metabolic disease. Botulinum toxin injections every 12 weeks are first-line for focal dystonia; trihexyphenidyl, baclofen, and deep brain stimulation of the globus pallidus interna are options for generalized or refractory disease. Tourette syndrome (childhood-onset motor and vocal tics, often with OCD and ADHD) and tardive dyskinesia from chronic dopamine receptor blockade (treated with valbenazine or deutetrabenazine) are additional movement disorders the scribe will encounter.

13 Dementia & Cognitive Disorders Degenerative

Mild cognitive impairment (MCI) is cognitive decline beyond normal aging without functional impairment. Dementia (major neurocognitive disorder) requires cognitive decline sufficient to impair independent function in daily activities.

Subtypes

• Alzheimer disease — insidious amnestic (hippocampal) onset, with progressive involvement of language, visuospatial, and executive domains. Biomarkers: CSF Aβ42 low / tau-p high, amyloid PET positive, MRI with hippocampal and medial temporal atrophy.
• Vascular dementia — stepwise decline, focal deficits, executive dysfunction, white-matter disease or prior strokes on imaging.
• Frontotemporal dementia (FTD) — behavioral variant (disinhibition, apathy, compulsions, hyperorality) or primary progressive aphasia variants (semantic, nonfluent). Onset often in 50s–60s.
• Dementia with Lewy bodies (DLB) — see section 11. Neuroleptics can produce severe reactions.
• Normal pressure hydrocephalus — covered in section 17.

Assessment & Treatment

Cognitive screens: MMSE (max 30, <24 suggests dementia; insensitive to MCI and executive dysfunction), MoCA (max 30, ≥26 normal; more sensitive to MCI, executive, visuospatial). Workup includes TSH, B12, RPR, HIV when indicated, MRI brain, and specialty testing (LP amyloid/tau, amyloid/tau PET) when biomarkers will change management. Symptomatic pharmacologic treatment: cholinesterase inhibitors (donepezil, rivastigmine, galantamine) and memantine (NMDA receptor antagonist) for moderate-to-severe Alzheimer. Disease-modifying anti-amyloid monoclonals lecanemab and donanemab are approved for early Alzheimer and require MRI surveillance for ARIA (amyloid-related imaging abnormalities — edema and microhemorrhages). AAN Practice Guideline on Mild Cognitive Impairment is a standard citation.

14 Peripheral Neuropathy Peripheral

Peripheral neuropathy can be classified by distribution (symmetric length-dependent polyneuropathy vs mononeuropathy multiplex vs plexopathy vs radiculopathy vs polyradiculoneuropathy), by fiber type (large fiber — vibration/proprioception/motor; small fiber — pain/temperature/autonomic), and by pathology (axonal vs demyelinating). The most common etiology in North America is diabetes mellitus, producing a classic distal symmetric sensorimotor polyneuropathy in a stocking-glove distribution. Other causes: B12 deficiency (subacute combined degeneration with dorsal column and corticospinal involvement), alcohol, thyroid disease, HIV, chemotherapy (platinum compounds like cisplatin/oxaliplatin, taxanes, vincristine, bortezomib), hereditary (Charcot-Marie-Tooth — most commonly CMT1A from PMP22 duplication), paraneoplastic (anti-Hu, anti-CV2), vasculitic (painful mononeuropathy multiplex, nerve biopsy diagnostic), heavy metals, amyloid (TTR, AL), and idiopathic.

Workup

Labs: A1C, B12 with MMA, TSH, CMP, CBC, SPEP/IFE (monoclonal gammopathy can cause demyelinating neuropathy), HIV, RPR; genetic testing for CMT if hereditary picture. EMG/NCS localizes and characterizes (axonal vs demyelinating). LP for inflammatory demyelinating cases.

GBS and CIDP

Guillain-Barré syndrome (GBS): acute (<4 weeks) ascending symmetric weakness, areflexia, variable sensory loss, often post-infectious (Campylobacter jejuni classically — associated with the AMAN variant and worse prognosis; also CMV, EBV, Zika, SARS-CoV-2, Mycoplasma). Subtypes include acute inflammatory demyelinating polyradiculoneuropathy (AIDP, most common in West), acute motor axonal neuropathy (AMAN), acute motor and sensory axonal neuropathy (AMSAN), and Miller-Fisher syndrome (ophthalmoplegia, ataxia, areflexia, anti-GQ1b antibodies). CSF shows albuminocytologic dissociation (high protein, normal cells) after the first week. Treat with IVIG 2 g/kg over 5 days or plasma exchange (5 sessions); they are equally effective — steroids do NOT help. Monitor forced vital capacity, negative inspiratory force, and bulbar function closely because respiratory failure requiring intubation occurs in ~25%. Autonomic dysfunction (arrhythmias, BP lability, ileus) is a common cause of morbidity. Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) evolves over >8 weeks with symmetric proximal and distal weakness, areflexia, sensory involvement; NCS shows demyelinating features. Treated with steroids, IVIG, SC Ig, or plasma exchange as first-line therapy.

Painful Neuropathy Treatment

First-line neuropathic pain agents: gabapentin, pregabalin, duloxetine, amitriptyline/nortriptyline. Topicals (lidocaine 5% patch, capsaicin 8% patch) add benefit. Avoid chronic opioids.

15 Neuromuscular Junction & Myopathies Neuromuscular

Myasthenia gravis (MG) is an autoimmune disease directed against postsynaptic acetylcholine receptors (AChR Ab positive in ~85% of generalized MG, ~50% of ocular MG) or MuSK (muscle-specific kinase, ~5–10%). A smaller subset is "seronegative." Hallmark is fatigable weakness — ptosis, diplopia, bulbar symptoms (dysarthria, dysphagia, nasal regurgitation), neck flexion weakness, and proximal limb weakness that worsens with activity and improves with rest and cold. Diagnosis relies on antibody testing, bedside ice pack test for ptosis, EMG with repetitive nerve stimulation (>10% decremental response) or single-fiber EMG (jitter), and CT chest for thymoma (present in ~10–15%).

Myasthenic crisis is life-threatening respiratory failure from progressive bulbar and respiratory muscle weakness, treated with IVIG or plasma exchange plus pulse steroids, ICU monitoring, and early intubation before CO2 retention (watch NIF ≤−20 and FVC ≤15–20 mL/kg). Medications to avoid in MG: aminoglycosides, fluoroquinolones, macrolides, beta blockers, magnesium, neuromuscular blockers, and telithromycin — each can precipitate crisis. Chronic therapy: pyridostigmine 30–60 mg q4–6h (acetylcholinesterase inhibitor — symptomatic only), prednisone (start low and titrate up to avoid early worsening), steroid-sparing immunosuppressants (azathioprine, mycophenolate mofetil, tacrolimus, methotrexate, cyclosporine), thymectomy (especially if thymoma, also beneficial in non-thymomatous AChR+ generalized MG per MGTX trial), and newer targeted biologics: eculizumab and ravulizumab (C5 complement inhibitors), efgartigimod and rozanolixizumab (FcRn antagonists). MGFA clinical classification ranges from I (ocular only) through V (intubated).

Lambert-Eaton myasthenic syndrome (LEMS) is a presynaptic disorder (voltage-gated calcium channel antibodies), often paraneoplastic from small-cell lung cancer (~60% of cases), with proximal weakness that paradoxically improves with brief exercise (facilitation), autonomic features (dry mouth, constipation, erectile dysfunction), and reduced or absent reflexes that augment after sustained contraction. EMG shows incremental response with rapid repetitive stimulation. Treatment: evaluate for underlying malignancy, 3,4-diaminopyridine (amifampridine), pyridostigmine, steroids, and immunosuppression.

Myopathies: inflammatory myositis (polymyositis, dermatomyositis with characteristic skin findings — heliotrope rash, Gottron papules, shawl sign; inclusion body myositis with finger-flexor and quadriceps weakness in older men; immune-mediated necrotizing myopathy with SRP or HMGCR antibodies) presents with proximal weakness and elevated CK (sometimes >10,000); EMG shows myopathic units with irritability (fibrillations, sharp waves); muscle biopsy confirms pathology; treated with steroids, IVIG, and steroid-sparing immunosuppression. Dystrophies (Duchenne, Becker, myotonic types 1 and 2, limb-girdle, FSHD) are typically hereditary and diagnosed with genetic testing. Statin-associated myopathy ranges from mild myalgia to rhabdomyolysis to immune-mediated necrotizing myopathy with anti-HMGCR antibodies — the last does not resolve with statin discontinuation and requires immunotherapy. Metabolic myopathies (McArdle, Pompe, mitochondrial) can present with exercise intolerance.

16 CNS Tumors & Neuro-Oncology Oncologic

Primary CNS tumors are classified per WHO with both histology and molecular features. Gliomas include astrocytomas, oligodendrogliomas, and glioblastoma — graded I–IV by WHO with molecular classification integrating IDH mutation status, 1p/19q codeletion (defining oligodendroglioma), ATRX loss, TERT promoter mutation, and MGMT promoter methylation (which predicts temozolomide response). Glioblastoma (WHO grade 4) is the most aggressive, with median survival of ~15 months despite maximal therapy. Meningiomas are usually benign extra-axial tumors arising from arachnoid cap cells and are often incidental findings on imaging. Schwannomas, particularly vestibular schwannoma (acoustic neuroma) at the cerebellopontine angle, present with unilateral sensorineural hearing loss, tinnitus, and disequilibrium. Other primary tumors include ependymoma, medulloblastoma (pediatric), pituitary adenoma, craniopharyngioma, and CNS lymphoma.

Metastatic disease is more common than primary CNS tumors overall — top sources are lung, breast, melanoma, renal, and GI. Mets are typically multiple and at gray-white junction, with prominent vasogenic edema. Leptomeningeal carcinomatosis presents with cranial neuropathies, radiculopathies, and communicating hydrocephalus; CSF cytology and MRI with gadolinium are diagnostic.

Presentations include headache (worse in morning, with Valsalva, progressive), focal deficits, new-onset seizures (up to 30% of brain tumor patients), and cognitive/personality change. Management is multidisciplinary across neurology, neurosurgery, radiation oncology, and medical oncology: dexamethasone for vasogenic edema (typically 4–16 mg/day), antiseizure medications if seizures occur (levetiracetam is preferred because it does not induce hepatic metabolism of chemotherapy), surgical maximal safe resection or biopsy, radiation (whole-brain, stereotactic radiosurgery, or fractionated), temozolomide for glioblastoma following the Stupp protocol, tumor-treating fields (TTF), and increasingly targeted therapies (BRAF/MEK inhibitors, EGFR inhibitors, immune checkpoint inhibitors) selected by molecular profile.

17 CNS Infections & Normal Pressure Hydrocephalus Infectious/CSF

CNS infections overlap with infectious disease, but neurologists are frequently consulted for diagnosis and management. Bacterial meningitis: fever, headache, neck stiffness, altered mental status; classic triad is present in fewer than half of cases, so a single sign plus fever is enough to trigger workup. Empiric therapy in adults is ceftriaxone + vancomycin + dexamethasone; add ampicillin for Listeria coverage in >50 yo, immunocompromised, pregnant, or alcohol use disorder. CSF: high WBC with neutrophilic predominance, low glucose (<40 or CSF/serum <0.4), high protein, positive Gram stain/culture. CT before LP is indicated for immunocompromise, new seizures, focal deficits, papilledema, or reduced GCS to avoid herniation risk.

Viral meningitis (enterovirus commonly) is self-limited — CSF shows lymphocytic pleocytosis, normal glucose, mildly elevated protein. Viral encephalitis (HSV-1 classically) presents with fever, behavioral/personality change, seizures, and temporal lobe findings on MRI; treat empirically with IV acyclovir 10 mg/kg q8h while awaiting CSF HSV PCR. Delaying acyclovir worsens outcomes — start it on suspicion.

Other important CNS infections: tuberculous meningitis (basilar enhancement, cranial neuropathies, hydrocephalus), neurocysticercosis (seizures with ring-enhancing or calcified cystic lesions in immigrants from endemic regions), cryptococcal meningitis (AIDS and other immunocompromised, elevated OP, positive cryptococcal antigen), toxoplasmosis (ring-enhancing lesions in AIDS), Lyme neuroborreliosis (facial palsy, radiculitis, aseptic meningitis), neurosyphilis (RPR and CSF VDRL), and progressive multifocal leukoencephalopathy (PML) from JC virus reactivation in immunocompromised, particularly natalizumab patients — always screen JC virus serology before starting natalizumab and during therapy.

Autoimmune encephalitis (anti-NMDA receptor, anti-LGI1, anti-CASPR2, GAD65, etc.) is an increasingly recognized mimic presenting with psychiatric symptoms, seizures, memory loss, and movement abnormalities; treat with immunotherapy (steroids, IVIG, plasma exchange, rituximab) and evaluate for underlying tumor (ovarian teratoma in anti-NMDA).

Normal pressure hydrocephalus (NPH) is the classic triad of gait apraxia ("magnetic" or "glue-foot" gait), urinary incontinence, and cognitive decline ("wet, wacky, wobbly"). MRI shows ventriculomegaly out of proportion to cortical atrophy (Evans index > 0.3). Large-volume LP (~30–50 mL removal) or external lumbar drainage trial assesses whether ventriculoperitoneal shunting will help — gait typically responds best, cognition least reliably.

18 Vertigo & Dizziness Vestibular

First distinguish vertigo (illusion of motion) from presyncope, disequilibrium, and non-specific dizziness. Then separate peripheral (inner ear/vestibular nerve) from central (brainstem/cerebellum) causes. The HINTS exam (Head Impulse, Nystagmus, Test of Skew) in acute vestibular syndrome is more sensitive than early MRI for posterior fossa stroke when performed by an experienced examiner. A "benign" HINTS pattern is: abnormal (positive, corrective saccade) head impulse, unidirectional horizontal nystagmus, and no vertical skew — consistent with peripheral cause. Any finding of normal head impulse, direction-changing nystagmus, or skew deviation suggests central etiology ("dangerous HINTS") and warrants urgent MRI and stroke workup.

Peripheral Vertigo

• BPPV — brief (< 1 min) positional vertigo from otoconia in semicircular canals. Diagnosed with Dix-Hallpike; treated with Epley maneuver.
• Vestibular neuritis — acute prolonged vertigo lasting days, often post-viral, without hearing loss. Labyrinthitis adds hearing loss. Short vestibular suppressants + early ambulation + vestibular rehab.
• Ménière disease — episodic vertigo lasting 20 minutes to hours with fluctuating low-frequency hearing loss, tinnitus, aural fullness. Low-salt diet, diuretics, intratympanic steroids or gentamicin for refractory disease.

Central vertigo (cerebellar/brainstem stroke, MS, tumor) — any vertical or direction-changing nystagmus, gait ataxia out of proportion to vertigo, or other brainstem findings warrants urgent MRI.

19 Neurologic Procedures & Diagnostics Procedural

Neurology is a largely diagnostic specialty, but a scribe will document a defined set of procedures performed in clinic, at the bedside, or in specialized labs.

20 Neuroimaging & Electrodiagnostics Diagnostic

NCCT head: first-line for stroke alert to rule out hemorrhage, SAH (up to 6 hours), skull fracture, large mass effect. CTA head and neck: evaluates for LVO, aneurysm, dissection, vasculitis. CT perfusion: estimates ischemic core and salvageable penumbra using CBF/CBV/Tmax maps — supports late-window thrombectomy decisions. MRI brain: DWI is the most sensitive sequence for acute infarct within minutes of onset; FLAIR shows edema and demyelination; T2*/SWI detects microbleeds and hemorrhage; T1 with gadolinium identifies active inflammation, blood-brain barrier breakdown, and tumors. MR angiography/venography: non-contrast time-of-flight or contrast-enhanced vascular imaging. Catheter angiography (DSA): gold standard for vascular anatomy and therapeutic access.

EEG Waveforms & Terms

You will hear phrases like: alpha rhythm (normal posterior dominant rhythm ~8–13 Hz), beta, theta, delta, spike-and-wave (epileptiform), generalized periodic discharges (GPDs), lateralized periodic discharges (LPDs), triphasic waves (metabolic encephalopathy), burst suppression (deep sedation, severe encephalopathy).

EMG/NCS Findings

Neurogenic/axonal: reduced CMAP amplitude with relatively preserved velocities; EMG shows fibrillation potentials, positive sharp waves, and large long-duration polyphasic motor units. Demyelinating: slow conduction velocities, prolonged distal latencies, conduction block, temporal dispersion. Myopathic: small short-duration polyphasic motor units with early recruitment. NMJ disorders: decrement on repetitive stimulation (MG, > 10% drop) or increment with rapid stimulation/exercise (LEMS).

21 Medications You Must Know Pharmacology

22 Classification & Scoring Systems Reference

23 Neurologic Physical Exam Reference

The neurologic exam is the most specialty-defining part of the note. Master the components and the documentation rhythm.

24 Abbreviations, Sample HPIs & References

Abbreviations — Diagnoses & Syndromes

Abbreviations — Procedures, Imaging & Exam

Abbreviations — Medications

Sample HPI Templates

References & Sources

Clinical Practice Guidelines

Landmark Clinical Trials

Diagram & Figure Sources