01Approach to the Critical Patient/attcp40

Immediate priorities

›Stroke protocol activation

›Activate when ipsilateral CN III palsy plus contralateral hemiataxia is recognized

›Time of last known well documented immediately

›IV alteplase window: within 4.5 hours of symptom onset

›Neurology consultation emergent

›All acute presentations require neurology

›If basilar artery involvement suspected, consider neurosurgery and neurointerventional

›Airway priority in obtunded patients

›GCS < 13 triggers immediate airway evaluation

›Brainstem strokes carry aspiration risk

Hemodynamic and neurological targets

›Blood pressure management targets

›If thrombolysis candidate: SBP < 185 mmHg and DBP < 110 mmHg prior to alteplase

›Labetalol IV 10-20 mg over 1-2 minutes or nicardipine infusion to achieve target

›Maintain SBP 180-185 mmHg during and 24 hours after alteplase

›If not thrombolysis candidate: permissive hypertension

›Allow SBP up to 220 mmHg unless end-organ damage evident

›Lower by no more than 15% in first 24 hours

›Hypotension in posterior circulation stroke indicates impending herniation

›SBP < 120 mmHg requires immediate intervention

›Neurological monitoring

›Neuro checks every 1-2 hours initially

›GCS, pupil exam, CN III assessment, limb coordination

›Continuous cardiac monitoring for atrial fibrillation detection

›AF is a cardioembolic source requiring anticoagulation

›Glucose target 7.8-10.0 mmol/l

›Both hypo- and hyperglycemia worsen stroke outcomes

02History/hx64

Core presenting syndrome

›Onset and timing

›Acute onset (seconds to minutes) — stroke until proven otherwise

›Last known well time — critical for thrombolysis eligibility

›Maximal at onset suggests embolic mechanism

›Subacute onset (hours to days) — mass, abscess, demyelination

›Progressive worsening over days to weeks suggests tumor or infection

›Cardinal symptoms

›Diplopia — typically vertical or oblique from CN III dysfunction

›Direction and onset of double vision

›Ptosis ipsilateral

›Unilateral vs bilateral

›Gait unsteadiness or limb incoordination contralateral

›Falling tendency

›Limb dysmetria on one side

Associated symptoms

›Additional brainstem symptoms

›Vertigo or nausea

›Posterior circulation involvement marker

›Dysarthria

›Corticobulbar or cerebellar involvement

›Dysphagia

›Aspiration risk assessment mandatory

›Headache

›Occipital or posterior — dissection or hemorrhage concern

›Neck pain or trauma

›Vertebral or basilar artery dissection

›Visual field deficits

03Physical Exam/exam56

Vital signs and general

›Hemodynamic snapshot

›Blood pressure — both arms if dissection suspected

›Asymmetry of 20 mmHg suggests subclavian or aortic pathology

›Heart rate and rhythm

›Irregularly irregular — atrial fibrillation

›Oxygen saturation

›Hypoxemia from aspiration or concurrent pulmonary pathology

›Temperature

›Fever raises infectious etiology concern

›General appearance

›Level of consciousness

›GCS documentation required at presentation

›Ability to protect airway

›Secretion management, gag reflex

Cranial nerve and ocular exam

›CN III examination ipsilateral

›Ptosis

›Partial ptosis from levator palpebrae dysfunction

›Extraocular movements

›Down and out position — superior rectus, inferior rectus, medial rectus paresis

›Impaired adduction, elevation, and depression

›Pupillary response

›Pupil-sparing is common in fascicular (intraparenchymal) lesions

›Pupil-involving CN III palsy raises concern for compressive aneurysm

›Presence of partial vs complete palsy

›Partial palsy increases diagnostic challenge — rule out isolated microvascular palsy

›Other cranial nerves

04Differential Diagnosis/ddx49

Midbrain crossed syndromes

›Competing midbrain syndromes

›Weber syndrome

›Ipsilateral CN III palsy plus contralateral hemiparesis

›No ataxia — cerebral peduncle involvement (ICD-10 G83.89)

›Benedikt syndrome

›Ipsilateral CN III palsy plus contralateral rubral tremor and hemiataxia

›Red nucleus involvement with or without SCP

›Nothnagel syndrome

›Ipsilateral CN III palsy plus bilateral cerebellar ataxia

›Tectal and SCP involvement

›Reverse Claude's syndrome

›Ipsilateral ataxia with CN III palsy from lesion at rostral SCP decussation

Isolated cranial nerve and cerebellar mimics

›Isolated CN III palsy etiologies

›Microvascular CN III palsy

›Pupil-sparing, pain may be present, resolves in 3 months

›No ataxia distinguishes from Claude's

›Posterior communicating artery aneurysm

›Pupil-involving CN III palsy is hallmark

›Headache common — emergent CTA or MRA required (ICD-10 I67.1)

›Cavernous sinus pathology

›Additional CN IV, VI, V1 involvement

›Proptosis, chemosis

›Cerebellar stroke without CN III palsy

›PICA territory infarction

›Ataxia, nystagmus, Horner syndrome, no CN III palsy (ICD-10 I63.5)

›SCA territory infarction

05Laboratory Tests/lt45

Core stroke labs

›Metabolic and hematologic panel

›Complete blood count

›Polycythemia as stroke risk

›Thrombocytopenia affects thrombolysis eligibility

›Basic metabolic panel

›Glucose — hypoglycemia as stroke mimic; target 7.8-10.0 mmol/l

›Renal function for contrast and medication dosing

›Coagulation studies

›PT/INR and aPTT — anticoagulant use and thrombolysis eligibility

›INR > 1.7 is a contraindication to IV alteplase

›Type and screen

›If hemorrhagic conversion or surgery anticipated

Cardioembolic and vascular risk workup

›Lipid and metabolic risk markers

›Fasting lipid panel

›LDL target for high-intensity statin therapy

›HbA1c

›Chronic glycemic control assessment

›Glucose tolerance status

›Inflammatory and infectious markers

›ESR and CRP

›Elevated in vasculitis, Behcet, or infectious etiology

›Blood cultures

›If fever present or infectious etiology suspected

›RPR/VDRL

›Neurosyphilis consideration in appropriate epidemiologic context

›Cardiac markers

06Diagnostic Tests/dt77

Scoring Systems

›NIHSS — National Institutes of Health Stroke Scale

›Quantifies stroke severity and guides treatment eligibility

›Scores 0-42; higher scores reflect greater deficit

›NIHSS 0-4: minor stroke; 5-15: moderate; 16-20: moderate-severe; 21+: severe

›Serial NIHSS tracks improvement or deterioration

›Document at presentation, post-thrombolysis, and at 24 hours

›Modified Rankin Scale (mRS)

›Baseline functional status assessment

›mRS 0: no symptoms; mRS 6: death

›Pre-stroke mRS required for thrombolysis eligibility assessment

›Follow-up functional outcome at 3 months — 77.7% of isolated midbrain infarction patients achieve mRS 2 or less

›ABCD2 Score — not validated for posterior circulation; use NIHSS instead

›NIHSS preferred for brainstem localization syndromes

›ABCD2 may underestimate posterior circulation TIA risk

MRI

›MRI brain with diffusion-weighted imaging (DWI)

›Gold standard for Claude's syndrome diagnosis

›Restricted diffusion in ventromedial midbrain at level of superior cerebellar peduncle

›Oculomotor nerve fascicle involvement visualized

›DWI identifies acute ischemia within minutes of onset

›Sensitivity for acute midbrain infarction superior to CT

›Posterior fossa artifact limits CT sensitivity for small midbrain infarcts

›FLAIR sequences

›Hyperintense signal evolves after 6-12 hours

›MS plaques, vasculitis signal on FLAIR

›T2 and T1 with and without contrast

›Ring enhancement — abscess, tuberculoma, neurocysticercosis, metastasis

›Cystic lesion with scolex — neurocysticercosis pathognomonic

›MRA head and neck

›Basilar artery stenosis or occlusion

›Vertebral artery hypoplasia — present in up to 77.7% of pure midbrain infarction patients

›Vertebral artery dissection

›Intimal flap, double lumen, narrowed lumen with enhancement

›Posterior communicating artery aneurysm

›If pupil-involving CN III palsy present

›Diffusion tensor imaging (DTI)

›Delineates specific tract involvement in variant presentations

›SCP decussation involvement in reverse Claude's syndrome

›Tectospinal tract integrity assessment

›Useful when clinical-radiological discordance exists

CT

›Non-contrast CT head

›First-line imaging to exclude hemorrhage

›Hemorrhagic conversion or hemorrhagic stroke requires alteplase exclusion

›CT insensitive for small midbrain infarcts — negative CT does not exclude ischemic Claude's syndrome

›Posterior fossa bone artifact

›Significantly limits sensitivity for brainstem pathology

›Sensitivity for midbrain infarction on CT: approximately 50-60% in first 24 hours

›CT angiography head and neck

›Large vessel occlusion assessment — basilar artery occlusion

›Basilar artery thrombosis is a life-threatening emergency requiring thrombectomy

›Vertebrobasilar stenosis and vessel anatomy

›Identifies posterior communicating artery aneurysm if pupil-involving CN III palsy

›Completed within minutes in most stroke centers

›Use as adjunct when MRI not immediately available

›CT perfusion

›Ischemic penumbra assessment in extended thrombolysis window

›4.5-24 hours if wake-up stroke or unknown onset time

›Mismatch between core infarct and penumbra guides intervention

Ultrasound

›Carotid and vertebral duplex ultrasound

›Vertebral artery flow assessment

›Retrograde flow in subclavian steal syndrome

›Vertebral artery hypoplasia identification

›Carotid intima-media thickness

›Atherosclerotic burden as cardioembolic workup adjunct

›Transcranial Doppler (TCD)

›Basilar artery flow velocity

›Elevated velocities suggest stenosis

›Microembolic signals

›Active cardioembolic source or paradoxical embolism through PFO

›Patent foramen ovale screening

›Bubble study with TCD or TTE/TEE

›Echocardiography

›TTE for structural cardiac source

›Wall motion abnormalities, valvular disease, intracardiac thrombus

›TEE if TTE non-diagnostic or high suspicion for cardioembolic source

›Left atrial appendage thrombus, aortic arch atheroma, PFO with atrial septal aneurysm

›Point-of-care cardiac ultrasound

›Expedited LV function and pericardial effusion assessment in unstable patients

07Disposition/dispo35

Admission criteria

›Admission indications

›All acute presentations of Claude's syndrome require hospital admission

›Stroke workup, monitoring, and secondary prevention initiation

›ICU admission criteria

›Fluctuating or deteriorating neurological deficits

›Basilar artery occlusion or involvement

›Large infarct on neuroimaging

›Post-IV alteplase monitoring required for 24 hours

›Impaired swallowing requiring aspiration precautions

›Stroke unit admission

›Stable minor deficit with completed acute workup

›Continuous cardiac monitoring capability required

Consultation requirements

›Mandatory consultations

›Neurology — all cases emergent

›MRI acquisition, thrombolysis decision, secondary prevention planning

›Neurointerventional radiology

›Basilar artery occlusion candidate for mechanical thrombectomy

›Neurosurgery

›Mass lesion, hemorrhage, or hydrocephalus identified

›Ophthalmology

›Persistent oculomotor palsy for long-term management

›Prism glasses or patching for diplopia management

›Oncology

›Metastatic etiology confirmed

›Infectious disease

›Neurocysticercosis, neuro-Behcet, or TB etiology

08Treatment/t89

Acute thrombolysis

›IV alteplase criteria

›Time window: within 4.5 hours of symptom onset or last known well

›AHA/ASA Class I recommendation for eligible patients

›Alteplase 0.9 mg/kg IV, maximum 90 mg

›10% of dose as IV bolus over 1 minute

›Remaining 90% as infusion over 60 minutes

›Key contraindications

›Active hemorrhage or hemorrhagic stroke on CT

›INR > 1.7 or recent anticoagulant use within therapeutic window

›Platelet count < 100 x 10^9/L

›BP > 185/110 mmHg uncontrolled despite treatment

›Post-alteplase monitoring

›Neuro checks every 15 minutes during infusion

›Every 30 minutes for 6 hours, then hourly until 24 hours

›Hold antithrombotic agents for 24 hours post-alteplase

Mechanical thrombectomy

›Thrombectomy criteria

›Basilar artery occlusion is primary indication in posterior circulation

›Extended window up to 24 hours with perfusion imaging mismatch (Class IIa)

›Large vessel occlusion on CTA or MRA

›NIHSS score and functional status guide eligibility

›Stent retriever or aspiration thrombectomy per neurointerventional team

›mTICI 2b or 3 recanalization as target

Blood pressure management

›Pre-thrombolysis BP management

›Labetalol IV 10-20 mg over 1-2 minutes

›Repeat every 10-20 minutes, maximum 300 mg total

›Nicardipine IV infusion 5 mg/hour

›Titrate by 2.5 mg/hour every 5-15 minutes

›Maximum 15 mg/hour

›Target SBP < 185 mmHg and DBP < 110 mmHg before alteplase

›Post-alteplase and non-thrombolysis BP management

›Maintain SBP < 180 mmHg and DBP < 105 mmHg for 24 hours post-alteplase

›Non-thrombolysis candidate: permissive hypertension up to 220 mmHg SBP

›Avoid aggressive lowering — impairs collateral perfusion

Secondary prevention — antiplatelet therapy

›Non-cardioembolic ischemic stroke

›Aspirin 325 mg oral loading dose, then 81 mg daily

›Initiate within 24-48 hours of onset (after alteplase if given)

›Class I recommendation — AHA/ASA Stroke Guidelines

›Dual antiplatelet therapy for high-risk TIA or minor stroke (NIHSS 3 or less)

›Aspirin 325 mg plus clopidogrel 300-600 mg loading, then clopidogrel 75 mg daily

›Duration: 21 days dual therapy, then single antiplatelet

›POINT and CHANCE trials support dual antiplatelet in minor stroke

›One case report documented Claude's syndrome resolution within 10 days with antiplatelet therapy alone

›Statin therapy

›High-intensity statin — atorvastatin 40-80 mg or rosuvastatin 20-40 mg daily

›Class I recommendation regardless of baseline LDL

›Initiated in all ischemic stroke patients

Secondary prevention — anticoagulation

›Cardioembolic source identified

›Atrial fibrillation

›Direct oral anticoagulants (DOACs) preferred over warfarin

›Apixaban 5 mg twice daily or rivaroxaban 20 mg daily or dabigatran 150 mg twice daily

›Initiate after hemorrhagic conversion excluded — typically 48-72 hours post-stroke

›Vertebrobasilar dissection

›Anticoagulation or antiplatelet therapy — no definitive superiority established

›Neurology-guided decision based on lesion characteristics

›Cardioembolic workup prior to anticoagulation

›30-day cardiac telemetry to detect paroxysmal AF

›Echocardiography for structural source

Etiology-specific treatment

›Neurocysticercosis

›Albendazole 7.5 mg/kg twice daily for 8-30 days (weight-based)

›Combined with dexamethasone 0.1-0.15 mg/kg/day to reduce inflammation

›Neurosurgery consultation for hydrocephalus or large cysts

›Neuro-Behcet disease

›High-dose IV methylprednisolone 1 g daily for 3-5 days

›Followed by oral prednisone taper

›Disease-modifying therapy — azathioprine or infliximab for recurrent disease

›Multiple sclerosis exacerbation

›IV methylprednisolone 1 g daily for 3-5 days

›Accelerates recovery, does not alter long-term disability

›Metastatic tumor

›Dexamethasone 10 mg IV loading, then 4 mg IV/oral every 6 hours

›Reduces peritumoral edema

›Radiation oncology and neurosurgery consultation

Supportive care

›Glycemic management

›Glucose target 7.8-10.0 mmol/l during admission

›Insulin infusion if persistently above 10.0 mmol/l

›Avoid hypoglycemia — worsens neurological outcomes

›Temperature management

›Normothermia target — treat fever aggressively

›Acetaminophen 650-1000 mg every 6 hours for fever

›External cooling if hyperthermia > 37.5 C

›Aspiration precautions

›Dysphagia screening before any oral intake

›Formal speech-language pathology assessment

›NPO until swallowing assessed

›Head of bed elevation 30-45 degrees

›Rehabilitation initiation

›Early physical therapy for gait and coordination

›Occupational therapy for fine motor and functional retraining

›Speech therapy for diplopia-related functional limitation

09Special Populations/sp60

Pregnancy

›Pregnancy considerations for Claude's syndrome

›Stroke in pregnancy — rare but serious

›Incidence of pregnancy-associated stroke approximately 30 per 100,000 deliveries

›Postpartum period carries highest risk

›Thrombolysis in pregnancy

›Alteplase is relatively contraindicated — limited case series data

›Individualized decision — life-threatening stroke may justify use

›Involve maternal-fetal medicine and neurology jointly

›MRI without gadolinium preferred in first trimester

›MRA can be performed without contrast for vascular assessment

›Antiplatelet therapy in pregnancy

›Low-dose aspirin generally considered safe

›Clopidogrel — limited safety data in pregnancy

›Anticoagulation for cardioembolic source in pregnancy

›Low molecular weight heparin preferred over warfarin

›DOACs are contraindicated in pregnancy

›Eclampsia and HELLP syndrome as stroke mimics

›Seizures with hypertension and proteinuria — diffuse cerebral vasospasm

Geriatric

›Geriatric-specific considerations

›Atypical and subtle presentations more common in older adults

›Truncal ataxia may be attributed to pre-existing deconditioning

›CN III palsy may be attributed to pre-existing microvascular disease

›Higher prevalence of vascular risk factors in elderly

›Hypertension, diabetes, atrial fibrillation — polypharmacy considerations

›Thrombolysis in elderly (over 80 years)

›IV alteplase can be used — AHA/ASA Class I if no contraindications

10Background/b58

Epidemiology

›Prevalence and incidence

›Claude's syndrome is exceedingly rare among brainstem stroke syndromes

›Prospective study of 308 brainstem stroke patients identified only 1 case of Claude's syndrome

›Classical crossed brainstem syndromes other than Wallenberg's syndrome are uncommon

›Most common etiology is cerebrovascular disease

›Small vessel disease and large vessel disease predominate

›Cardioembolic etiology also documented

›Non-vascular etiologies documented in case reports

›Malignancy, neurocysticercosis, neuro-Behcet disease, demyelination

›Named after French neurologist Henri Claude — first described in early 20th century

›Prognosis data

›77.7% of patients with isolated midbrain infarction achieve mRS 2 or less at 3 months

›Pure midbrain infarction carries favorable functional prognosis

›One case resolved completely within 10 days with antiplatelet therapy alone

›Vertebrobasilar hypoplasia found in up to 77.7% of isolated midbrain infarction patients

›Suggests hemodynamic mechanism in significant proportion

Pathophysiology

›Neuroanatomical substrate

›Lesion location: ventromedial midbrain

›Involves superior cerebellar peduncle (SCP) and adjacent oculomotor nerve fascicles

›SCP carries cerebellar outflow from dentate nucleus to contralateral red nucleus and thalamus

›CN III fascicular involvement

›Oculomotor nerve fascicles traverse the midbrain tegmentum adjacent to the SCP

›Fascicular lesions commonly spare the pupil — Edinger-Westpupil fibers are peripheral on the nerve

›SCP decussation anatomy

›SCP fibers cross in the midbrain before synapsing in contralateral red nucleus and VL thalamus

›Lesion caudal to decussation → contralateral hemiataxia (classical Claude's)

›Lesion rostral to decussation → ipsilateral ataxia (reverse Claude's syndrome)

›Vascular anatomy

›Perforating branches of posterior cerebral artery (PCA) and basilar artery supply ventromedial midbrain

›Paramedian perforators from the interpeduncular segment of PCA

›Anteromedial and anterolateral perforators from basilar artery apex

›Vertebrobasilar hypoplasia increases hemodynamic vulnerability

›Reduced autoregulatory reserve in the posterior circulation territory

›Distinction from related syndromes

›Weber syndrome — cerebral peduncle + CN III fascicles → adds corticospinal tract involvement

›Results in contralateral hemiparesis absent in Claude's

›Benedikt syndrome — red nucleus + CN III fascicles → rubral tremor added

›Overlap exists — spectrum of ventromedial midbrain injury

Therapeutic Considerations

›Evidence base for acute treatment

›IV alteplase for posterior circulation stroke

›AHA/ASA Class I recommendation within 4.5-hour window

›Posterior circulation strokes were included in major thrombolysis trials

›Mechanical thrombectomy for basilar artery occlusion

›BEST and BASICS trials demonstrated benefit — Class IIa recommendation

›Extended window up to 24 hours with appropriate patient selection

›Dual antiplatelet therapy for minor stroke and TIA

›POINT and CHANCE trials: NNT approximately 29 to prevent recurrent stroke

›Secondary prevention evidence

›High-intensity statin therapy reduces recurrent stroke by approximately 16%

›Class I recommendation for all ischemic stroke patients

›Anticoagulation for AF-associated stroke reduces recurrence by 64% versus no therapy

›DOACs non-inferior or superior to warfarin with lower intracranial hemorrhage

›Blood pressure lowering reduces stroke recurrence by 30-40%

›Target SBP < 130 mmHg for most patients long-term

›Etiology-specific evidence

›Neurocysticercosis treatment: albendazole plus corticosteroids reduces cyst burden and seizure recurrence

›Neuro-Behcet: corticosteroids in acute phase, immunosuppressants for prevention

›Demyelination: methylprednisolone hastens recovery but does not alter long-term disability

11Patient Discharge Instructions/pdi43

copy discharge instructions

›What is Claude's syndrome

›Claude's syndrome is a rare type of stroke affecting a small area deep in the brainstem called the midbrain

›It causes drooping of one eyelid and double vision on one side

›It also causes difficulty with balance and coordination on the opposite side of the body

›The most common cause is a blood clot blocking a small artery in the brainstem

›Other causes include tumors, infections, or inflammation

›Your medications

›Take all prescribed medications as directed every day

›Blood thinners (aspirin, clopidogrel) help prevent another stroke

›Statins lower cholesterol and reduce stroke risk

›Blood pressure medications protect your blood vessels

›Do not stop any medication without speaking to your doctor

›Keep a medication list with you at all times

›Activity and safety

›Do not drive until cleared by your neurologist

›Eye and balance problems make driving unsafe

›Use a cane or walker if balance is impaired

›Remove trip hazards at home

›Eye patching or prism glasses may help with double vision — follow ophthalmology instructions

›Follow-up appointments

›Neurology appointment within 1-2 weeks — keep this appointment

›Ophthalmology appointment for persistent eye problems

›Primary care physician within 1 week to check blood pressure and medications

›Return to emergency department immediately if

›Sudden new or worsening weakness in arms or legs

›Sudden new or worsening double vision or vision loss

›Sudden severe headache — worst headache of your life

12References/r26

Guidelines and key sources

›Primary literature — Claude's syndrome case series and imaging

›Broadley SA, Taylor J, Waddy HM, Thompson PD. The Clinical and MRI Correlate of Ischaemia in the Ventromedial Midbrain: Claude's Syndrome. Journal of Neurology. 2001. PMID 12013587

›Established MRI as gold standard and described ventromedial midbrain localization

›Seo SW, Heo JH, Lee KY, et al. Localization of Claude's Syndrome. Neurology. 2001. PMID 11756616

›Documented IV alteplase use and case of full resolution in 10 days with antiplatelet therapy

›Marx JJ, Thomke F. Classical Crossed Brain Stem Syndromes: Myth or Reality? Journal of Neurology. 2009. PMID 19252797

›Prospective cohort of 308 brainstem stroke patients — only 1 classical Claude's case identified

›Song TJ, Suh SH, Cho H, Lee KY. Claude's Syndrome Associated With Neurocysticercosis. Yonsei Medical Journal. 2010. PMID 20879071

›Documented non-vascular etiology — ring-enhancing cystic lesion

›Bateman JR, Murty P, Forbes M, et al. Pupil-Sparing Third Nerve Palsies and Hemiataxia: Claude's and Reverse Claude's Syndrome. Journal of Clinical Neuroscience. 2016. PMID 26883351

›Described reverse Claude's syndrome and pupil-sparing variant

›Amano E, Komatuzaki T, Ishido H, et al. Pitfalls in the Diagnosis of Pupil-Sparing Oculomotor Nerve Palsy Without Limb Ataxia: Variant of Claude's Syndrome and DTI Analysis. Journal of Clinical Neuroscience. 2018. PMID 29066240

›Diffusion tensor imaging delineating tract involvement in atypical Claude's

›Yavuz P, Solmaz I, Kaya UA, et al. Claude Syndrome in Childhood Associated With Probable Neuro-Behcet Disease. Neuropediatrics. 2023. PMID 36564024

›Pediatric etiology — inflammatory/vasculitic mechanism

›Gilberti N, Gamba M, Costa A, et al. Pure Midbrain Ischemia and Hypoplastic Vertebrobasilar Circulation. Neurological Sciences. 2014. PMID 23852316

›Vertebrobasilar hypoplasia in 77.7% of pure midbrain infarction patients

›Bogousslavsky J, Maeder P, Regli F, Meuli R. Pure Midbrain Infarction: Clinical Syndromes, MRI, and Etiologic Patterns. Neurology. 1994. PMID 7969955

›Foundational study of midbrain infarction spectrum

›Stroke treatment guidelines

›Powers WJ, et al. 2019 AHA/ASA Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke. 2019

›Class I recommendation for alteplase within 4.5 hours

›Mechanical thrombectomy indications

›Blood pressure management targets

›Rigual R, Fuentes B, Diez-Tejedor E. Management of Acute Ischemic Stroke. Medicina Clinica. 2023. PMID 37532617

›Contemporary acute stroke management review

Evidence & Review

Evidence & Review