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Benedikt's SyndromeMANAGEMENT

SYSTEMIC AND MISCELLANEOUS PRESENTATIONS · 12 SECTIONS

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782 items

☷ Legend

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Cardiovascular Presentations71▾

Respiratory Presentations52▾

Neurological Presentations83▾

Gastrointestinal Presentations74▾

Genitourinary and Reproductive Presentations48▾

Infectious Disease Presentations148▾

Trauma Presentations89▾

Toxicologic Presentations80▾

Psychiatric Presentations26▾

Musculoskeletal and Rheumatologic Presentations96▾

Dermatology Presentations23▾

Environmental and Exposure Presentations27▾

Hematologic and Oncologic Presentations36▾

Pediatric-Specific Presentations19▾

Endocrine and Metabolic Presentations45▾

ENT and Maxillofacial Presentations27▾

Ophthalmologic Presentations19▾

Obstetric Presentations23▾

Systemic and Miscellaneous Presentations17▾

Allergic Transfusion Reaction Anaphylaxis Angioedema Benedikt's Syndrome Cannabis-induced hyperemesis Eczema (acute flare)Gradenigo's Syndrome Horner's Syndrome (Acute)Huntington's Disease (Acute Presentation)Kanavel's Signs Lemierre's Syndrome Procedural sedation Radiation exposure Retained products of conception Sever's Disease Urticaria Venous air embolism

01Approach to the Critical Patient/attcp44

Immediate priorities

›Acute posterior circulation stroke recognition

›Sudden-onset ipsilateral CN III palsy with contralateral deficits

›Diplopia and ptosis onset time documentation

›Last known well time for thrombolytic eligibility

›Posterior circulation ischemic stroke until proven otherwise

›Basilar or posterior cerebral artery perforator occlusion most common etiology

›CT head immediately to rule out hemorrhage

›If within treatment window, activate stroke team immediately

›IV alteplase eligibility assessment

›Endovascular thrombectomy candidacy per AHA/ASA guidelines

Airway and hemodynamic stabilization

›Airway threats in midbrain stroke

›Depressed consciousness with basilar artery involvement

›GCS trend monitoring

›If GCS < 8, definitive airway management

›Dysphagia and aspiration risk

›NPO until formal swallow evaluation

›Brainstem involvement increases aspiration risk

›Rapidly declining consciousness

›Suggests brainstem compression or basilar artery occlusion

›Emergent neurology and neurosurgery consultation

›Hemodynamic targets in acute ischemic stroke

›Blood pressure permissive hypertension if not thrombolysis candidate

›SBP < 220 mmHg and DBP < 120 mmHg threshold

›Avoid aggressive lowering in first 24 hours

›If thrombolysis or thrombectomy candidate

›SBP < 185 mmHg and DBP < 110 mmHg before and during treatment

02History/hx64

Presenting symptoms

›Core syndrome onset

›Diplopia and binocular horizontal or vertical separation

›Acute versus progressive onset

›Time of onset documentation

›Ptosis of ipsilateral eyelid

›Complete versus partial ptosis

›Associated pupil dilation

›Contralateral limb weakness

›Upper and lower extremity involvement

›Functional impact on ambulation

›Movement disorder symptoms

›Contralateral intention tremor

›Worsening with purposeful movement

›Holmes tremor latency days to months after initial insult

›Gait instability and falls

›Hemiataxia pattern

›Dysmetria on self-report

›Involuntary movements characterization

›Low frequency 3 to 5 Hz pattern

›Present at rest and with posture and with intention

Alarm features

›High-risk historical red flags

›Thunderclap headache at symptom onset

›Aneurysmal subarachnoid hemorrhage concern

›Basilar artery hemorrhage concern

›Recent head or neck trauma

›Vertebral artery dissection risk

03Physical Exam/exam65

Cranial nerve and ocular examination

›CN III palsy findings ipsilateral to lesion

›Ptosis

›Partial versus complete

›Levator palpebrae involvement

›Down and out eye position

›Unopposed superior oblique and lateral rectus action

›Impaired adduction elevation and depression

›Pupil assessment

›Mydriasis when parasympathetic fibers involved

›Pupil-sparing pattern suggests microvascular etiology

›Additional ocular findings

›Vertical gaze abnormalities

›Involvement of adjacent midbrain structures

›Parinaud syndrome overlap when dorsal midbrain affected

›Nystagmus assessment

›Torsional or vertical nystagmus in brainstem lesions

›Direction and plane characterization

Motor and cerebellar examination

›Contralateral motor findings

›Upper motor neuron pattern weakness

›Hemiparesis face arm and leg

›Increased tone and spasticity

›Hyperactive deep tendon reflexes

›Pathologically brisk compared to ipsilateral side

›Positive Babinski sign

›Pronator drift assessment

›Subtle hemiparesis detection

04Differential Diagnosis/ddx51

Life-threatening mimics

›Posterior communicating artery aneurysm

›ICD-10 I67.1 intracranial aneurysm

›Isolated CN III palsy typically pupil-involving

›No contralateral signs unless rupture or large mass effect

›Thunderclap headache as distinguishing feature

›Emergent CTA or LP required

›Neurosurgical consultation

›Basilar artery occlusion

›ICD-10 I63.02 cerebral infarction due to basilar artery occlusion

›May present with bilateral findings

›Decreased consciousness and locked-in syndrome risk

›High mortality without emergent reperfusion

Midbrain stroke syndrome differentials

›Weber syndrome

›ICD-10 G46.3 brain stem stroke syndrome

›Ipsilateral CN III palsy and contralateral hemiparesis

›Cerebral peduncle lesion without red nucleus involvement

›No tremor or ataxia distinguishing from Benedikt

›Lesion localization

›Ventral midbrain predominantly

›Spares red nucleus

›Claude syndrome

›Ipsilateral CN III palsy and contralateral hemiataxia

›Red nucleus and superior cerebellar peduncle lesion

›No hemiparesis distinguishing from Benedikt

›Lesion localization

›Dorsal tegmentum predominantly

05Laboratory Tests/lt48

Acute stroke workup

›Mandatory initial labs

›Complete blood count

›Thrombocytopenia affecting thrombolytic eligibility

›Polycythemia as stroke risk factor

›Coagulation studies PT INR aPTT

›Anticoagulant effect assessment

›INR > 1.7 contraindicates alteplase

›Serum glucose

›Hypoglycemia mimicking stroke excluded

›Target glucose 7.8 to 10 mmol/l in acute stroke

›Basic metabolic panel

›Electrolyte disturbances affecting CNS function

›Renal function for contrast and medication dosing

Vascular risk and etiology workup

›Cardiac workup

›Troponin

›Cardiac comorbidity and Takotsubo association with stroke

›Elevated in 20% of large strokes

›12-lead ECG

›Atrial fibrillation detection as embolic source

›QTc prolongation baseline for medication planning

›Lipid and metabolic panel

›Fasting lipid panel

›LDL target assessment for secondary prevention

›Statin initiation planning

›HbA1c

›Chronic glycemic control assessment

06Diagnostic Tests/dt99

Scoring Systems

›Acute stroke severity and eligibility tools

›NIHSS National Institutes of Health Stroke Scale

›Standardized neurological deficit quantification

›Score 0 to 42 with higher scores indicating greater severity

›Guides thrombolysis and thrombectomy eligibility

›Serial assessment for trajectory monitoring

›mRS modified Rankin Scale

›Baseline functional status documentation

›Score 0 to 6 with 6 indicating death

›Pre-stroke mRS guides treatment and goals of care

›ASPECTS Alberta Stroke Program Early CT Score

›Applied to posterior circulation on CTA source images

›Extent of ischemic change in posterior circulation

›pc-ASPECTS for posterior fossa territory

›Holmes tremor severity tools

›Fahn-Tolosa-Marin Tremor Rating Scale

›Tremor amplitude and frequency quantification

›Functional disability scoring

›Used to track pharmacologic treatment response

MRI

›MRI brain indications and protocol

›Gold standard for acute midbrain infarction

›DWI shows restricted diffusion in tegmentum at red nucleus and cerebral peduncle level

›ADC map confirms restricted diffusion

›Sensitivity for acute posterior circulation infarct superior to CT

›FLAIR sequence

›Subacute and chronic infarct delineation

›White matter lesion burden assessment for demyelination

›DWI-FLAIR mismatch supports acute ischemia within 4.5 hours

›T2 and T1 with gadolinium

›Tumor characterization

›Rim-enhancing abscess pattern

›Active demyelinating plaques enhance with gadolinium

›MRA for vascular assessment

›MRA head and neck

›Basilar artery stenosis or occlusion

›Posterior cerebral artery perforator territory assessment

›Vertebral artery dissection detection

›Limitations

›Longer acquisition time than CT

›Motion artifact in agitated patients

›Small perforator vessel resolution limited

›Specialized MRI sequences

›Diffusion tensor imaging DTI

›Cerebellothalamic tract disruption demonstration

›Nigrostriatal pathway injury assessment

›Guides prognosis for Holmes tremor development

›Susceptibility-weighted imaging SWI

›Microhemorrhage detection

›Cavernous malformation identification

›Amyloid angiopathy screening

›Non-contrast CT head

›First-line acute imaging

›Hemorrhage exclusion before thrombolysis

›Completed in minutes

›Limited sensitivity for small acute midbrain infarcts

›CT findings in acute midbrain infarction

›Often normal in first 6 hours

›Subtle hypodensity developing over hours to days

›Posterior fossa posterior circulation territory hypodensity

›CT angiography head and neck

›Preferred in acute setting for speed and sensitivity

›Basilar artery occlusion identification

›Posterior cerebral artery stenosis or occlusion

›Vertebral artery stenosis or dissection

›CTA interpretation

›Filling defect or vessel cutoff

›Collateral circulation assessment

›Contrast considerations with renal function

›CT perfusion

›Penumbra and core infarct assessment

›Mismatch pattern guides thrombectomy candidacy

›CBF and CBV and Tmax maps

›May be limited in posterior fossa due to beam hardening artifact

Ultrasound

›Carotid duplex ultrasound

›Extracranial carotid and vertebral artery assessment

›Vertebral artery flow and direction

›Subclavian steal syndrome detection

›Plaque burden and stenosis

›Limitations for posterior circulation

›Intracranial vessels not directly visualized

›Basilar artery not assessable

›Operator-dependent quality

›Transcranial Doppler TCD

›Posterior circulation flow assessment

›Basilar artery peak systolic velocity

›Posterior cerebral artery stenosis detection

›Embolic signal monitoring

›Patent foramen ovale bubble study

›Right to left shunt detection

›Cryptogenic stroke evaluation in younger patients

›Echocardiography

›Transthoracic echocardiogram TTE

›Cardioembolic source evaluation

›LV thrombus and wall motion abnormality

›Valvular disease assessment

›Transesophageal echocardiogram TEE

›PFO characterization with shunt quantification

›Left atrial appendage thrombus detection

›Aortic arch atheroma evaluation

07Disposition/dispo34

Acute admission criteria

›All confirmed posterior circulation strokes require admission

›Neurology or stroke unit admission

›Telemetry monitoring for atrial fibrillation

›Serial neurological examinations

›Blood pressure management protocols

›ICU or stroke unit level care indications

›Basilar artery occlusion or large territory infarction

›Declining level of consciousness GCS < 13

›Post-thrombolysis or post-thrombectomy monitoring

Transfer criteria

›Transfer to comprehensive stroke center

›Thrombectomy eligibility at non-thrombectomy capable center

›Posterior circulation large vessel occlusion

›Within treatment window

›Drip and ship protocol activation

›Complex management needs

›Neurosurgical consultation for hemorrhagic transformation

›Interventional neuroradiology access required

Follow-up planning

›Inpatient milestones before discharge

›Etiology workup completed

›Cardiac monitoring minimum 24 hours for paroxysmal atrial fibrillation

›Vascular imaging reviewed

›Swallow safety cleared or modified diet initiated

›Speech language pathology consultation

›Dysphagia management plan

›Rehabilitation assessment

08Treatment/t117

Acute reperfusion therapy

›IV thrombolysis with alteplase

›Eligibility criteria

›Ischemic stroke within 4.5 hours of last known well

›No contraindications including hemorrhage on CT

›SBP < 185 mmHg and DBP < 110 mmHg before initiation

›Dosing protocol

›0.9 mg/kg IV maximum 90 mg total

›10% as bolus over 1 minute

›Remaining 90% as infusion over 60 minutes

›Post-thrombolysis monitoring

›BP every 15 minutes for 2 hours then every 30 minutes for 6 hours

›Neurological checks every 15 minutes during infusion

›Hold antiplatelets and anticoagulants for 24 hours

›Endovascular thrombectomy

›Candidacy criteria

›Large vessel occlusion on CTA

›Baseline mRS 0 to 1 (functionally independent pre-stroke)

›Posterior circulation thrombectomy up to 24 hours with favorable perfusion imaging

›Class I recommendation for anterior circulation per AHA/ASA

›Growing evidence supports posterior circulation benefit

›Basilar artery occlusion may warrant attempt beyond standard window

Blood pressure management

›Pre-thrombolysis target

›Labetalol IV

›10 to 20 mg IV over 1 to 2 minutes

›Repeat every 10 minutes to maximum 300 mg

›Hold if bradycardia or bronchospasm

›Nicardipine IV infusion

›Initial 5 mg/hour

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

›Maximum 15 mg/hour

›Post-thrombolysis or post-thrombectomy target

›SBP < 180 mmHg and DBP < 105 mmHg for 24 hours

›Labetalol or nicardipine infusion continued as needed

›Avoid hypotension to protect penumbra

›Non-thrombolysis permissive hypertension

›SBP < 220 mmHg unless hemorrhagic transformation

›Reassess at 24 hours for initiation of long-term management

Antithrombotic therapy

›Antiplatelet therapy for non-cardioembolic stroke

›Aspirin

›325 mg loading dose within 24 to 48 hours of symptom onset

›81 mg daily for long-term secondary prevention

›Class I recommendation AHA/ASA

›Dual antiplatelet therapy

›Aspirin 81 mg plus clopidogrel 75 mg daily

›High-risk TIA or minor stroke 21-day course evidence-based

›POINT and CHANCE trials supporting 21-day dual therapy

›Clopidogrel loading

›300 to 600 mg loading dose when indicated

›75 mg daily maintenance

›Anticoagulation for cardioembolic stroke

›Atrial fibrillation etiology

›Direct oral anticoagulant preferred over warfarin

›Apixaban 5 mg twice daily or rivaroxaban 20 mg daily

›Timing of initiation based on infarct size and hemorrhagic risk

›Warfarin when direct oral anticoagulants contraindicated

›Target INR 2 to 3

›Bridge with heparin if high thromboembolic risk

Holmes tremor management

›First-line pharmacologic trial

›Levodopa-carbidopa

›Effective in approximately 54% of patients with Holmes tremor

›Starting dose 25/100 mg three times daily with food

›Titrate gradually over weeks to effective dose

›Maximum dose determined by response and tolerability

›Trihexyphenidyl anticholinergic

›Commonly used adjunct to levodopa

›Starting 1 mg daily titrated to 2 to 5 mg three times daily

›Avoid in elderly due to cognitive side effects

›Second-line options

›Pramipexole dopamine agonist

›May augment levodopa response

›Starting 0.125 mg three times daily

›Titrate over weeks per tolerability

›Levetiracetam

›Reported benefit in selected cases

›500 mg twice daily starting dose

›Titrate to 1500 to 3000 mg daily in divided doses

›Clonazepam adjunct

›0.5 mg twice daily for tremor amplitude reduction

›Sedation and falls risk monitoring

›Deep brain stimulation for refractory Holmes tremor

›Thalamic VIM nucleus target

›Considered when pharmacologic failure

›Movement disorder specialist evaluation required

›Subthalamic nucleus target alternative

›Outcomes

›60 to 80% tremor reduction reported in case series

›Best results when combined dopaminergic and thalamic pathway treatment

›Medications to avoid

›Valproate worsens tremor

›Aggravates essential tremor and Holmes tremor

›Metoclopramide and typical antipsychotics

›Dopamine blockade worsens Holmes tremor

›Use alternative antiemetics

Secondary stroke prevention

›Statin therapy

›High-intensity statin initiation

›Atorvastatin 40 to 80 mg daily

›LDL target < 1.8 mmol/l for atherosclerotic etiology

›Class I recommendation for ischemic stroke

›Rosuvastatin alternative

›20 to 40 mg daily

›Hepatic function monitoring

›Antihypertensive management

›Initiate or resume antihypertensives at 24 hours if hemodynamically stable

›Target SBP < 130 mmHg for secondary prevention

›ACE inhibitor or ARB plus thiazide diuretic preferred

›Lifestyle modification counseling

›Low-sodium diet

›Mediterranean-style diet pattern

›Risk factor modification

›Smoking cessation counseling and pharmacotherapy

›Varenicline or nicotine replacement

›Diabetes glycemic control

›HbA1c target individualized

›Coordinate with endocrinology

›Atrial fibrillation rate and rhythm control

›Cardiology referral for rate control optimization

›Anticoagulation compliance reinforcement

09Special Populations/sp91

Pregnancy

›Pregnancy-specific considerations

›Stroke risk increased during pregnancy and puerperium

›Hypercoagulable state of pregnancy

›Peripartum cardiomyopathy as embolic source

›Preeclampsia and HELLP syndrome vasculopathy

›Thrombolysis in pregnancy

›Alteplase is FDA category C

›Relative contraindication due to hemorrhagic risk

›May be considered for severe disabling stroke after multidisciplinary discussion

›Imaging approach

›MRI preferred over CT to avoid ionizing radiation

›Gadolinium contrast generally avoided in first trimester

›CTA if MRA unavailable and diagnosis critical

›Antithrombotic selection in pregnancy

›Low molecular weight heparin preferred over warfarin

›Enoxaparin 1 mg/kg subcutaneously twice daily

›Does not cross placenta

›Warfarin teratogenic in first trimester

›Aspirin generally safe in pregnancy

›Low-dose 81 mg daily

›Avoid near term due to bleeding risk

›Direct oral anticoagulants contraindicated in pregnancy

›Cross placenta and risk fetal harm

›Switch to LMWH when pregnancy confirmed

›Fetal monitoring and delivery planning

›Fetal monitoring when viable gestation

›Coordinate with obstetrics and maternal-fetal medicine

›Delivery timing individualized

›Breastfeeding considerations

›Warfarin and LMWH compatible with breastfeeding

›Avoid direct oral anticoagulants while breastfeeding

Geriatric

›Geriatric-specific features

›Higher prevalence of vascular risk factors

›Hypertension most significant

›Atrial fibrillation prevalence increases with age

›Atypical presentation common

›Cognitive baseline confusion affecting NIHSS interpretation

›Pre-existing gait impairment masking new ataxia

›Frailty assessment impacts treatment goals

›Pre-stroke mRS documentation critical

›Goals of care discussion early in admission

›Medication considerations in geriatric patients

›Trihexyphenidyl for Holmes tremor

›Avoid due to anticholinergic cognitive side effects

›Urinary retention and falls risk

›Levodopa preferred for Holmes tremor in elderly

›Lower starting doses

›Monitor for orthostatic hypotension

›Anticoagulation in elderly with atrial fibrillation

›CHA2DS2-VASc score typically high

›Fall risk does not outweigh stroke prevention benefit

›Direct oral anticoagulants preferred for reduced intracranial hemorrhage risk

›Rehabilitation and disposition

›Inpatient rehabilitation candidacy

›Functional gains expected with therapy

›Goals of care alignment

›Swallowing and nutrition priority

›Dysphagia more prevalent with brainstem stroke in elderly

›PEG tube consideration for prolonged dysphagia

Pediatrics

›Pediatric posterior circulation stroke considerations

›Etiology differs from adults

›Arterial dissection more common

›Cardiac embolism from congenital heart disease

›Vasculitis and hypercoagulable states

›Clinical recognition challenge

›Ataxia and tremor overlap with cerebellar tumors

›Pediatric midbrain tumors on differential

›MRI preferred for diagnosis without radiation

›Thrombolysis in pediatric stroke

›Alteplase not formally approved for pediatric use

›Case-by-case multidisciplinary decision

›Pediatric neurology consultation required

›Evidence limited to case series and registry data

›Weight-based dosing if used

›0.9 mg/kg maximum 90 mg

›Same protocol as adult adjusted for weight

›Holmes tremor in pediatric patients

›Levodopa-carbidopa approach

›Start at lower doses with slow titration

›Dosing approximately 3 to 5 mg/kg/day of levodopa in divided doses

›Pediatric movement disorder consultation

›Neoplastic etiology must be excluded

›Brainstem glioma or pilocytic astrocytoma

›Gadolinium-enhanced MRI

›Rehabilitation in pediatric patients

›Neuroplasticity advantage over adults

›Earlier and more intensive rehabilitation

›Constraint-induced movement therapy consideration

›School and developmental support

›Educational accommodation planning

›Developmental pediatrics referral

10Background/b88

Epidemiology

›Incidence and prevalence

›Benedikt syndrome is rare

›Exact incidence not well-established due to rarity

›Among all midbrain stroke syndromes it is infrequent

›More common than Claude syndrome, less common than Weber syndrome

›Age and demographics

›Predominantly adult presentation

›Reflects posterior circulation stroke demographics

›Mean age of posterior circulation stroke approximately 63 to 68 years

›Etiology distribution

›Posterior circulation ischemic stroke most common

›Basilar artery perforator occlusion

›Posterior cerebral artery P1 segment perforators

›Hypertension-related small vessel disease predominant

›Other etiologies

›Intracranial hemorrhage into midbrain tegmentum

›Tumor including metastatic and primary brainstem glioma

›Demyelination in younger populations

›Trauma including penetrating injury and closed head injury

›Iatrogenic after basilar aneurysm clipping reported

›Holmes tremor epidemiology

›Develops in subset of patients with midbrain lesions

›Median latency approximately 2 months from lesion onset

›Range from days to years

›Exact prevalence in Benedikt syndrome not established

Pathophysiology

›Lesion anatomy

›Tegmentum of the midbrain at red nucleus level

›Ipsilateral oculomotor nucleus or CN III fascicles

›Ipsilateral red nucleus

›Ipsilateral cerebral peduncle corticospinal tract

›Clinical-anatomic correlation

›CN III fascicle involvement causes ipsilateral CN III palsy

›Red nucleus disruption causes contralateral hemiataxia

›Cerebral peduncle involvement causes contralateral hemiparesis

›Vascular anatomy

›Perforating arteries from basilar and posterior cerebral arteries

›Paramedian midbrain perforators from basilar artery

›Posteromedial choroidal artery from P1 segment

›Small vessel arteriolar disease from hypertension

›Posterior circulation vulnerability

›Limited collateral circulation to brainstem perforators

›Perforators are end-arteries with no anastomotic backup

›Holmes tremor pathophysiology

›Combined dopaminergic and cerebellothalamic pathway disruption

›Nigrostriatal dopaminergic denervation from midbrain lesion

›Dentatorubrothalamic tract disruption from red nucleus involvement

›Dual pathway lesion required for Holmes tremor generation

›Latency of Holmes tremor onset

›Reflects time for transsynaptic degeneration of dopaminergic neurons

›Dopamine transporter SPECT DaTscan demonstrates nigrostriatal denervation

›Median 2 month latency supports degeneration mechanism

›Tremor characteristics

›Low frequency 3 to 5 Hz distinguishes from essential tremor

›Present at rest and with posture and with intention

›Amplitude increases with target-directed movements

Therapeutic Considerations

›Acute reperfusion rationale

›Time-to-treatment window critical

›Posterior circulation stroke may have longer reperfusion window than anterior

›Some centers extend to 24 hours with favorable perfusion imaging

›Basilar artery occlusion mortality very high without reperfusion

›Posterior circulation thrombectomy evidence

›BASICS trial and BEST trial inform practice

›Ongoing trials refining candidacy criteria

›Multidisciplinary discussion required for complex cases

›Holmes tremor treatment rationale

›Dual pathway target for treatment

›Dopaminergic replacement with levodopa addresses nigrostriatal denervation

›Approximately 54% response rate to levodopa

›Anticholinergic and GABAergic agents address non-dopaminergic component

›DaTscan utility

›Dopamine transporter imaging confirms nigrostriatal denervation

›Positive DaTscan predicts levodopa response

›Guides pharmacologic selection

›DBS as salvage therapy

›VIM thalamus stimulation for refractory tremor

›Significant functional improvement in published case series

›Reserved for patients failing comprehensive pharmacologic trials

›Secondary prevention evidence base

›Hypertension control strongest modifiable risk factor

›ACE inhibitor plus thiazide combination reduces recurrent stroke

›PROGRESS trial underpins combination treatment

›Statin therapy for secondary prevention

›SPARCL trial: atorvastatin 80 mg reduced recurrent stroke by 16%

›Benefit extends to posterior circulation ischemic stroke

›Atrial fibrillation anticoagulation

›ARISTOTLE and ROCKET AF support direct oral anticoagulants

›Reduced intracranial hemorrhage versus warfarin

›Class I recommendation for non-valvular atrial fibrillation

11Patient Discharge Instructions/pdi48

copy discharge instructions

›What happened to you

›You had a stroke affecting the brainstem affecting a region called the midbrain

›This caused weakness and coordination problems on one side of your body

›This also caused eye movement problems on the other side

›You may develop a tremor weeks or months from now

›This is called Holmes tremor and is related to your stroke

›It is treatable so report it immediately to your doctor

›Medications

›Take all medications exactly as prescribed

›Blood thinners or aspirin to prevent another stroke

›Blood pressure medications every day

›Cholesterol medications every day

›Do not stop any stroke medication without calling your doctor first

›Missing doses increases stroke recurrence risk

›If prescribed levodopa for tremor

›Take with food to reduce nausea

›Do not stop suddenly without medical advice

›Activity and safety

›Do not drive until cleared by your neurologist

›Eye movement problems and tremor affect driving safety

›Fall prevention measures at home

›Remove trip hazards

›Use assistive devices if recommended

›Grab bars in bathroom

›Swallowing precautions if applicable

›Follow diet texture recommended by speech therapist

›Sit upright for all meals

12References/r33

Guidelines and key sources

›Stroke guidelines

›AHA/ASA Guidelines for the Early Management of Patients with Acute Ischemic Stroke 2019

›Thrombolysis and thrombectomy eligibility criteria

›Blood pressure management targets

›AHA/ASA Secondary Prevention of Stroke Guidelines 2021

›Antithrombotic therapy recommendations

›Risk factor modification targets

›European Stroke Organisation ESO Guidelines

›Posterior circulation stroke specific guidance

›Mechanical thrombectomy for basilar artery occlusion

›Benedikt syndrome clinical references

›Benedikt syndrome original description and anatomic localization literature

›Topographic correlation of CN III palsy hemiataxia and hemiparesis

›Differentiation from Weber and Claude syndromes

›Holmes tremor mechanistic and treatment studies

›Duprez et al and Raina et al on levodopa response rates in Holmes tremor

›DaTscan utility for predicting levodopa response

›Deep brain stimulation outcomes in refractory Holmes tremor

›Evidence summaries

›BASICS trial: endovascular therapy for basilar artery occlusion

›New England Journal of Medicine 2021

›No significant benefit over medical management in primary analysis

›BEST trial: basilar artery occlusion endovascular trial

›Trends toward benefit in pre-specified subgroups

›POINT and CHANCE trials supporting dual antiplatelet therapy

›21-day dual antiplatelet for high-risk TIA and minor stroke

›SPARCL trial statin therapy for secondary stroke prevention

Learn More: Benedikt's Syndrome→

Comprehensive Clinical Review

Structured, evidence-informed, long-form analysis for deeper understanding.

Evidence & Review

Reviewed by SymptomDx Medical Team · Last reviewed August 18, 2026

SymptomDx is an educational tool for medical professionals. It does not replace clinical judgment. Verify all clinical data and drug dosages with authoritative sources.