Brainstem Ischemic Stroke Syndromes  

Brainstem Ischemic Stroke Syndromes 

Definition

• Stroke is the interruption of blood supply to a portion of the brain, leading to neuronal death and subsequent functional deficits.

Synonyms

• Stroke
• Brain attack
• Cerebrovascular accident (very vague, not commonly used)

ICD-10CM CODES
G46.3	Brain stem stroke syndrome
G46.7	Other lacunar stroke syndromes
I63.0	Cerebral infarction due to thrombosis of precerebral artery
I63.1	Cerebral infarction due to embolism of precerebral arteries
I63.12	Cerebral infarction due to embolism of basilar artery
I63.2	Cerebral infarction due to unspecified occlusion or stenosis of precerebral arteries
I63.6	Cerebral infarction due to cerebral venous thrombosis, nonpyogenic
I63.8	Other cerebral infarction
I63.9	Cerebral infarction, unspecified

Introduction

• The brainstem is commonly divided into three distinct territories: The medulla, the pons, and the midbrain.
• The brainstem is responsible for establishing a neuroanatomic connection between the body and the diencephalon, cerebellum, and neocortex.
• It is also the location of the majority of cranial nerve nuclei (excluding CNs I, II, and XI).
• Despite being a conduit for such vital functions as sensory input, motor output, coordination, alertness, and autonomic regulation, the diameter of the medulla is approximately 1.3 cm, less than the diameter of a dime (1.8 cm).
• Therefore, even relatively small infarcts or hemorrhages can devastate a patient’s functional status and result in severe long-term disability and death. Timely recognition of brainstem strokes with appropriate, rapid intervention is vital to optimize chances for a favorable long-term recovery.

Epidemiology & Demographics

Incidence

• •795,00 strokes per year in the U.S. ^1 , 2
• •10% of ischemic strokes involve the brainstem. ³
• •It is the third leading cause of death annually, with an estimated 137,000 deaths per year. ⁴
• •The odds of stroke doubles every 10 yr after the age of 55. ⁴
• •Compared to whites, stroke incidence is 2 to 4 times higher in Blacks and twice as high in Latinos.

Prevalence

• •2.7% to 3% of the population in the U.S. has experienced a stroke.

Predominant Sex & Age

• •Age is a nonmodifiable risk factor for stroke.
• •Stroke incidence is 24% to 30% higher in men. However, absolute annual stroke incidence is similar between genders, as women have a slightly longer life expectancy. ¹

Stroke Risk Factors

• •Hypertension
• •Diabetes mellitus
• •Atrial fibrillation
• •Hyperlipidemia
• •Tobacco use
• •Cocaine use
• •Methamphetamine use
• •Alcohol abuse
• •Obesity
• •Cardiac structural/conduction abnormalities
• •Chronic kidney disease
• •Obstructive sleep apnea
• •Poor diet
• •Vasculitis affecting the CNS
• •HIV-positive status

Stroke in the pediatric population is often caused by arterial dissection (number one cause), sickle cell disease, arteriovenous malformations, and vasculitides.

Nonmodifiable Risk Factors

• •Age
• •Gender
• •Genetic predisposition

Genetics

• •Having a first-degree relative with a stroke doubles stroke risk.
• •Studies have shown that risk for stroke is two times higher when stroke is experienced among first-degree relatives. ¹
• •While most strokes are caused by acquired risk factors, some genetic conditions predispose to stroke ( Box 1 ).BOX 1Inherited and Miscellaneous Disorders Causing Cerebral InfarctionFrom Jankovic J et al: Bradley and Daroff’s neurology in clinical practice, ed 8, Philadelphia, 2022, Elsevier.

Table

Homocystinuria Fabry disease Marfan syndrome Ehlers-Danlos syndrome Pseudoxanthoma elasticum Sneddon syndrome Hereditary hemorrhagic telangiectasia Neoplastic angioendotheliomatosis Susac syndrome Eales disease Reversible cerebral segmental vasoconstriction syndrome Hypereosinophilic syndrome Cerebral amyloid angiopathy Coils and kinks Arterial dolichoectasia Complications of coarctation of the aorta Air, fat, amniotic fluid, bone marrow, and foreign particle embolism

Pontine Infarcts

Pontine strokes make up 12% of posterior circulation infarcts.

Lateral pontine strokes:

• 1.Anterior inferior cerebellar artery (AICA) stroke:
  • a.Infarction of the middle cerebellar peduncle and lateral pons (affecting both the facial and vestibulocochlear nerves as well as the spinal trigeminal tract and spinothalamic tract)
  • b.Findings:
    • (1)I/L features: Facial weakness, loss of facial pain/temperature sensation, vertigo, hearing loss, limb ataxia
    • (2)C/L features: Body pain/temperature loss
• 2.Marie-Foix syndrome (lateral pontine syndrome)
  • a.Occlusion of the perforating branches off of the basilar artery as well as AICA
  • b.Findings:
    • (1)I/L features: Facial weakness, loss of facial pain/temperature sensation, vertigo, hearing loss, limb ataxia
    • (2)C/L features: Body pain/temperature loss, hemiparesis

Medial pontine strokes:

The following syndromes are all unified by an I/L abducens palsy with C/L hemiparesis, but are further differentiated based on their additional features:

• 1.Raymond syndrome:
  • a.Occlusion of branches off the basilar artery
  • b.Findings:
    • (1)I/L abducens nerve palsy.
    • (2)C/L hemiparesis. The “classic” variant can rarely include contralateral lower facial paresis.
• 2.Millard-Gubler syndrome:
  • a.Occlusions of branches off the basilar affecting the ventral aspect of the caudal pons
  • b.Findings:
    • (1)I/L features: Facial weakness (presents similar to Bell palsy, as the CN VII nucleus/nerve fascicle is damaged) and loss of the corneal reflex with esotropia (CN VI palsy)
    • (2)C/L features: Hemisensory loss and hemiparesis
• 3.Foville syndrome:
  • a.Occlusion of the paramedian branches of the basilar artery
    • (1)Findings:
      • (a)I/L features: Facial weakness and horizontal gaze palsy to side of the lesion due to involvement of the paramedian pontine reticular formation (PPRF)
      • (b)C/L features: Body hemisensory loss with hemiparesis

Bilateral stroke:

• 1.Locked-in syndrome:
  • a.Occlusion of the basilar artery
  • b.Findings: Perhaps the most functionally devastating stroke presentation with infarction of bilateral pontine structures
    • (1)B/L corticospinal tract involvement results in quadriplegia
    • (2)B/L PPRF involvement results in complete horizontal gaze palsy while sparing only vertical eye movements
    • (3)B/L facial nerve involvement as well as corticobulbar tract involvement results in facial paralysis and aphonia ( Table 2 )

Table

TABLE 2

Pontine Stroke Features

Modified from Ortiz de Mendivil A et al: Brainstem stroke: anatomy, clinical and radiological findings, Semin Ultrasound CT MR 34(2):131-141, 2013, https://doi.org/10.1053/j.sult.2013.01.004 .

Structure Involved	Corresponding Deficit(s)
Anteromedial pontine stroke:
Corticobulbar tract	Dysarthria, C/L facial palsy
Corticospinal tract	C/L hemiparesis
Corticopontine tract	C/L ataxia, pseudobulbar affect
Medial lemniscus	C/L loss of position sense and vibration
Medial longitudinal fasciculus	I/L internuclear ophthalmoplegia
CN VI nucleus	I/L lateral rectus palsy
CN VII fibers	I/L facial weakness
PPRF	I/L horizontal gaze paresis
Anterolateral pontine stroke:
Corticospinal tract	C/L hemiparesis
Spinothalamic tract	C/L loss of body pain and temperature sensation
Dorsolateral pontine stroke:
Caudal pons:
Lateral corticospinal tract	C/L hemiparesis (leg > arm)
Spinal trigeminal nucleus of CN V	I/L loss of facial pain and temperature
Middle cerebellar peduncle
CN VII fibers/nucleus	I/L facial weakness
CN VIII	Central hearing loss
Rostral pons:
Sympathetic tract	I/L Horner syndrome
Spinothalamic tract	C/L loss of body pain and temperature sensation
Superior cerebellar peduncle	C/L ataxia
Bilateral pontine stroke (locked in):
Corticospinal tract	Quadriplegia
Corticobulbar tract	Aphonia, dysphagia
PPRF	B/L horizontal gaze paresis
CN VII fibers/nuclei	B/L facial paralysis
Reticular formation	Reduced level of consciousness

C/L, Contralateral; CN, cranial nerve; I/L, ipsilateral; PPRF, paramedian pontine reticular formation.

Medullary Infarcts

Medullary infarcts account for 7% of brainstem infarcts, with lateral medullary infarcts three to five times more common than medial infarcts. ⁵

• 1.Wallenberg syndrome:
  • a.Lateral medullary syndrome caused by occlusion of the posterior inferior cerebellar artery (PICA). Infarct damages the nucleus ambiguus, spinal trigeminal nucleus, inferior cerebellar peduncle, and vestibular nuclei.
  • b.Findings:
    • (1)Vertigo, N/V, hiccups, hoarse voice, dysphagia, dysarthria. Less commonly noted features can include autonomic instability, even respiratory arrest (“Ondine curse”).
    • (2)I/L findings: Loss of facial temperature/pain sensation and Horner syndrome. Patient often falls to the side of the lesion when attempting to walk due to ataxia rather than weakness.
    • (3)C/L findings: Loss of body temperature/pain sensation. Uvular deviation will also be to the opposite side of infarct (this is due to I/L palatal weakness).
• 2.Dejerine syndrome:
  • a.Medial medullary syndrome caused by anterior spinal artery occlusion
  • b.Findings:
    • (1)I/L hypoglossal palsy (tongue deviates to side of infarct)
    • (2)C/L hemiparesis and loss of body touch and vibration sense (in clinical practice, touch and vibration sense may have a more variable distribution, as the medulla is the location of the decussating fibers that carry these sensory modalities)
• 3.Babinski-Nageotte syndrome:
  • a.Occlusion of the intracranial portion of the vertebral artery leads to both anterior spinal artery and PICA occlusions
  • b.Findings: Combination of lateral and medial medullary syndromes ( Table 3 )

TABLE 3

Medullary Stroke Features

Modified from Ortiz de Mendivil A et al: Brainstem stroke: anatomy, clinical and radiological findings, Semin Ultrasound CT MR 34(2):131-141, 2013, https://doi.org/10.1053/j.sult.2013.01.004 .

Structure Involved	Corresponding Deficit(s)
Medial anterior stroke (Dejerine):
Corticobulbar tract	Dysarthria
Corticospinal tract	C/l hemiparesis
Medial lemniscus	C/L loss of position sense and vibration
CN XII nucleus	I/L genioglossus weakness
Lateral medullary stroke (Wallenberg):
Spinal trigeminal tract	I/L loss of facial temperature and pain
Lateral spinothalamic tract	C/L body loss of pain and temperature sensation
Inferior cerebellar peduncle	I/L ataxia
Vestibular nuclei	Vertigo, with nausea and vomiting
Sympathetic fibers	I/L Horner syndrome
Nucleus ambiguus	Dysphagia, dysarthria, hoarse voice

C/L, Contralateral; CN, cranial nerve; I/L, ipsilateral.

Etiology

• •Small vessel disease (arteriosclerosis) leading to vascular occlusion of perforating branches of large arteries of the posterior circulation
• •Large vessel occlusion
• •Thromboembolic from large artery embolizing distally
• •Cardioembolic
• •Vertebral artery dissection
• •Additional miscellaneous and hereditary causes of stroke can be found in Box 1

Differential Diagnosis

• •Subarachnoid hemorrhage
• •Subdural hemorrhage
• •Intracerebral hemorrhage
• •Hemiplegic migraine
• •Seizure with Todd paralysis
• •Multiple sclerosis
• •Neuromyelitis optica
• •Neurosarcoidosis
• •Neuro-Behcet
• •TB meningitis
• •Fungal meningitis
• •Carcinomatous meningitis
• •Peripheral cranial nerve lesions
• •Conversion disorder

Laboratory tests

• •CBC
• •CMP
• •PT/PTT/INR
• •Lipid panel
• •HgA1C
• •In patients <55 or those without common stroke risk factors, thrombophilia/coagulopathy labs should also be considered ( Box 2 ) with a focus on arterial hypercoagulability (beta 2-glycoprotein, cardiolipin antibodies, and lupus anticoagulant) rather than on venous hypercoagulability (unless the patient has evidence of a right-to-left shunt such as a patent foramen ovale)BOX 2Specialized Laboratory Tests for ThrombophiliaFrom Jankovic J et al: Bradley and Daroff’s neurology in clinical practice, ed 8, Philadelphia, 2022, Elsevier.

Table

Antithrombin activity Protein C Protein S (total and free antigen levels) Activated protein C resistance Factor V Leiden Prothrombin gene (G20210 A) mutation Cardiolipin (IgG, IgM) antibodies β2-Glycoprotein 1 (IgG, IgM) antibodies Lupus anticoagulant Fibrinogen Plasminogen Plasminogen activator inhibitor Plasmin functional activity Factors V, VII, VIII, IX, X, XI, and XIII levels Hemoglobin electrophoresis Plasma homocysteine

TABLE 4

Imaging Modalities for Stroke

Imaging Modality	Advantages	Disadvantages
Magnetic resonance angiography	1.Excellent view of the large arteries of the neck and brain2.No contrast material needed	1.Cannot be performed in patients who are critically ill, who are unable to tolerate supine positioning, who have a pacemaker or other ferromagnetic hardware, or who are claustrophobic
Magnetic resonance perfusion	1.Assesses cerebral hemodynamics2.May show ischemic penumbra (i.e., the area of the brain that may be saved by timely intervention)	1.Not commonly available2.Not well standardized
CT angiography	1.Excellent view of the large arteries of the neck and brain2.Similar to magnetic resonance angiography with regard to resolution	1.Requires intravenous contrast
CT perfusion	1.Assesses cerebral hemodynamics2.May show ischemic penumbra (i.e., the area of the brain that may be saved by timely intervention)	1.Challenging to interpret in some cases2.Not routinely available at many facilities3.Requires intravenous contrast

CT, Computed tomography.

Treatment

Recanalization

• •IV thrombolysis within 4.5 h of last known well and no contraindications, either IV alteplase or IV tenecteplase (TNK) can be offered ( Box 3 )BOX 3Eligibility Criteria for Acute Thrombolysis in Acute Ischemic StrokeFrom Rabinstein AA: Update on treatment of acute ischemic stroke. Continuum (Minneap Minn) 26(2):268-286, 2020, https://doi.org/10.1212/CON.0000000000000840 .

Table

Eligibility Criteria

•Diagnosis of ischemic stroke causing measurable and “disabling” neurologic deficit •The neurologic signs should not be minor and isolated. Caution should be exercised in treating a patient with major deficits •Onset of symptoms <4.5 h before beginning treatment •The neurologic signs should not be clearing spontaneously •The symptoms of stroke should not be suggestive of subarachnoid hemorrhage •The patient or family members should understand the potential risks and benefits from treatment

Contraindications for Thrombolysis (per AHA 2019 Guidelines)

•Severe head trauma in the last 3 mo •Ischemic stroke within 3 mo •Current intracranial hemorrhage •Prior intracranial hemorrhage (though risk benefit discussion can be had based on size of stroke as well as etiology) •Suspected subarachnoid hemorrhage •Intracranial intraaxial neoplasm •Suspected endocarditis •Recent intracranial/intraspinal surgery in last 3 mo•GI malignancy or GI bleed in last 21 days •Active internal bleeding •Elevated blood pressure (systolic >185 mm Hg and diastolic >110 mm Hg) •Evidence of active bleeding or acute trauma (fracture) on examination •Taking an oral anticoagulant within 48 h or, if taking warfarin, INR ≥1.7 is a contraindication•If receiving heparin in previous 48 h, aPTT must be in normal range •Platelet count ≤100,000 mm 3 •Seizure with postictal residual neurologic impairments•CT shows an extensive infarction (hypodensity >one third cerebral hemisphere)

Mechanical thrombectomy: For large vessel occlusion presenting within 24 h of last known well with CT perfusion (for those presenting between 6 and 24 h of last known well) demonstrating salvageable brain tissue in the territory of the LVO ( Box 4 )

BOX 4

Candidates for Mechanical Thrombectomy

From Rabinstein AA: Update on treatment of acute ischemic stroke, Continuum (Minneap Minn) 26(2):268-286, 2020, https://doi.org/10.1212/CON.0000000000000840 .

Table

• Age >18 h
• •NIHSS score ≥6
• •Time from symptom onset to groin puncture <6 h (can be extended up to 24 h if evidence of sizeable ischemic penumbra on CT perfusion imaging)
• •Good prestroke functional status
• •Alberta stroke program early CT score ≤6 on baseline CT scan
• •Presence of proximal intracranial artery occlusion

Antiplatelet Therapy

• •Aspirin (81 to 325 mg/day) within 48 h of stroke onset has been shown to decrease the likelihood of a repeat ischemic stroke. ⁶
• •Patients who have received IV thrombolysis should not be given antithrombotic or anticoagulant agents within the first 24 h after administration. If neuroimaging 24 h after tPA administration does not show evidence of hemorrhagic conversion, antiplatelet therapy should be initiated.

Anticoagulation Therapy

• •Atrial fibrillation or cardiac thrombus: Long-term anticoagulation is the standard of care for long-term recurrent stroke prevention.
• •In acute setting, therapeutic anticoagulation with heparin infusion vs. low-molecular-weight heparin for patients with cardioembolic stroke due to atrial fibrillation should be avoided due to relatively high risk of hemorrhagic conversion and little evidence to suggest any benefit.
• •The timeframe for when anticoagulation is started is largely dependent on the size of the infarct (longer delay for larger strokes) and evidence of hemorrhagic conversion on subsequent imaging.
• •Vascular risk factor modification: Chronic treatment of hypertension, hyperlipidemia, and diabetes mellitus.
• •Hypertension:
  • 1.In the acute setting, blood pressure management varies depending on several factors. Permissive hypertension (SBP up to 220 mm Hg) is allowed for the first 48 h after stroke unless the patient received thrombolysis. Thrombolysis requires a blood pressure below 185/110 mm Hg.
  • 2.Hypotension is a bad prognostic sign in an acute stroke.
  • 3.Chronically, achieving normal blood pressure is a significant stroke risk reduction strategy.

Hypoglycemia/hyperglycemia

• •Both hypo- and hyperglycemia have the potential to mimic stroke. Hypoglycemia and acute ischemic stroke can occur in tandem. In the event that neurologic deficits remain after glucose correction, continued acute stroke management, including potential tPA/thrombectomy, may need to be pursued.
• •Hyperglycemia should be treated with sliding-scale insulin, taking into consideration the patient’s oral intake during time in the ICU. The presence of hyperglycemia worsens ischemic stroke outcomes, but recent evidence has shown that aggressive treatment with an insulin pump does not improve outcomes. Overall, the goal glucose in the ICU is typically recommended to be kept between 100 and 180 mg/dl.

Fever

• •Fever is harmful during acute stroke and can worsen functional outcomes. Ascertaining and addressing the cause while lowering an elevated temperature is strongly advised.

Elevated Intracranial Pressure

• •Edema from larger cerebellar strokes or strokes near the fourth ventricle/cerebral aqueduct can cause CSF obstruction, leading to obstructive hydrocephalus.
• •Patients with large posterior circulation infarcts require close, frequent neurologic monitoring in the NICU.
• •Sedating medications (e.g., opioids, benzodiazepines) should be limited in order to ensure a consistent examination and so that early signs of hydrocephalus (encephalopathy, nausea, vomiting) can be noted early.
• •If impending CSF obstruction is a concern, the patient should be evaluated by neurosurgery, and a potential preventative suboccipital craniectomy vs. catheter placement for CSF diversion can be discussed before an emergent situation arises.

Disposition

• •Neurologic ICU for 24 h for patients who underwent either thrombolysis or thrombectomy

Chronic Rx ⁸

Post-stroke rehabilitation services continue to be the mainstay for functional recovery in stroke patients. Physical and occupational therapy combined with speech language pathology implemented early in patient care improve functional outcomes.

• •Spontaneous motor improvement can be seen over 1 to 3 mo.
• •Aphasia, hemineglect, and cognitive deficits can improve up to 1 yr after infarction. ⁷
• •Speech and language pathology can treat post-stroke dysphagia and dysarthria.

Complementary & Alternative Medicine

Future pharmacologic approaches

• •Growth factors and stem cell–based therapies are a potentially exciting future treatment option for stroke rehabilitation. However, these therapies are currently in the research and investigational stages.

Nonpharmacologic approaches

• •Transcranial magnetic stimulation (TMS) is currently being investigated to determine if there can be added benefit to functional outcome.

Referral

• •Comprehensive stroke center in acute period
• •Neurology
• •Cardiology
• •Neurosurgery
• •Critical care medicine
• •Interventional neuroradiology
• •Physical medicine and rehabilitation
• •Physical therapy
• •Occupational therapy
• •Speech language pathology

Prevention

Between 80% and 90% of strokes are preventable with proper risk factor modification. ⁶

Blood pressure ( Table 5 ): Goal of <130/80

TABLE 5

Blood Pressure Goals in Acute Ischemic Stroke

From Warshaw G et al: Ham’s primary care geriatrics, ed 7, Philadelphia, 2022, Elsevier.

Scenario	Blood Pressure Goal
Not a candidate for thrombolysis	BP <220/110 mm Hg
If candidate for alteplase/TNK	BP <185/110 mm Hg
Blood pressure for first 24 hr after alteplase/TNK	BP< 180/105 mm Hg
After thrombectomy	BP <140/80 mm Hg

TNK, Tenecteplase.

Antiplatelet therapy:

For noncardioembolic strokes, daily aspirin is correlated with a 13% reduction in relative risk for stroke. ⁶ Clopidogrel and prasugrel are alternative agents that can be used if aspirin is not tolerated. Dual antiplatelet therapy is appropriate in some patients for a short period of time, but is not recommended longer than 90 days because of an increased risk of major bleeding without additional benefit.

Anticoagulation

Secondary prevention of cardioembolic strokes requires anticoagulation ( Table 6 ).

• •Direct oral coagulants are preferred therapy for stroke risk reduction.
• •Other sources of cardioembolism such as mechanical heart valve require warfarin therapy.

TABLE 6

The CHA2DS2VASc Score

Condition/Risk Factor	Score
Congestive heart failure	+1
Hypertension	+1
Age >75	+2
Diabetes mellitus	+1
History of stroke or TIA	+2
Other vascular risk factor (e.g., peripheral arterial disease, MI)	+1
Age 65-74	+1
Female	+1

TIA, Transient ischemic attack.

Lipid-lowering therapy

• •Goal LDL value of <70 mg/dl is commonly targeted following stroke using high-intensity statin therapy (atorvastatin 40 to 80 mg or rosuvastatin 20 to 40 mg).

Glycemic control

• •Intense management of blood glucose following stroke has been difficult to correlate with a long-term reduction in recurrent stroke risk.
• •Avoid intense blood glucose control, as the risk of hypoglycemia outweighs the benefit.

Patient & Family Education:

Family members can play a vital role in ensuring the best long-term outcomes for stroke patients. Not only can they ensure medications are being properly taken but that rehabilitation is being completed and a healthy lifestyle is being pursued. Family can also assist with key surveillance metrics such as blood pressure and glucose monitoring.

Pearls & Considerations

• •Brainstem strokes can commonly present with crossed signs on examination.
• •The Modified Rankin Score ( Table 7 ) and The National Institute of Health Stroke Scale (NIHSS) ( Table 8 ) does not assess for a majority of classic posterior circulation deficits. Therefore when seeing signs such as vertigo, dysphagia, nausea/vomiting, and falling on examination, do not rule out stroke just because the NIHSS is misleadingly low.

TABLE 7

The Modified Rankin Scale

Score	Description
0	No symptoms.
1	No significant disability. Able to carry out all usual activities, despite some symptoms.
2	Slight disability. Able to look after own affairs without assistance, but unable to carry out all previous activities.
3	Moderate disability. Requires some help, but able to walk unassisted.
4	Moderately severe disability. Unable to attend to own bodily needs without assistance, or unable to walk unassisted.
5	Severe disability. Requires constant nursing care and attention, bedridden, incontinent.
6	Dead.

TABLE 8

The National Institutes of Health Stroke Scale (NIHSS)

1A. Level of Consciousness (LOC)	1B. LOC Questions	1C. LOC Commands
0 = Alert 1 = Not alert, but arousable 2 = Not alert, obtunded 3 = Coma	Ask the month and his/her age. 0 = Answers both correctly 1 = Answers one correctly 2 = Answers neither correctly	Open and close the eyes. Open and close the nonparetic hand. 0 = Performs both tasks correctly 1 = Performs one task correctly 2 = Performs neither task correctly
2. Best Gaze (Horizontal)	3. Visual Fields	4. Facial Palsy
0 = Normal 1 = Partial gaze palsy 2 = Forced deviation or total gaze paresis	0 = No visual loss 1 = Partial hemianopia 2 = Complete hemianopia 3 = Bilateral hemianopia	0 = Normal 1 = Minor paralysis 2 = Partial paralysis (total or near total paralysis of lower face) 3 = Complete paralysis of upper and lower face
5. Motor Arm	6. Motor Leg	7. Limb Ataxia
Right Arm extended with palms down 90 degrees (if sitting) or 45 degrees (if supine) for 10 sec 0 = No drift 1 = Drift; limb drifts down from position and does not hit bed or support in 10 sec 2 = Some effort against gravity 3 = No effort against gravity 4 = No movement Left	Right Leg extended at 30 degrees, always tested supine for 5 sec 0 = No drift 1 = Drift; limb drifts down from position and does not hit bed or support in 5 sec 2 = Some effort against gravity 3 = No effort against gravity 4 = No movement Left	The finger-nose-finger and heel-shin tests 0 = Absent 1 = Present in one limb 2 = Present in two limbs
8. Sensory	9. Best Language	10. Dysarthria
To Pinprick or Noxious Stimuli 0 = Normal 1 = Mild to moderate sensory loss 2 = Severe to total sensory loss	0 = No aphasia, normal 1 = Mild-to-moderate aphasia 2 = Severe aphasia 3 = Mute, global aphasia, coma	0 = Normal 1 = Mild-to-moderate 2 = Severe (including mute/anarthric due to aphasia); do not score if intubated
11. Extinction and Inattention		Total Score: 0-42
0 = No abnormality1 = Present2 = Profound (two modalities)

References

1.Furie K.: Epidemiology and primary prevention of stroke . Continuum (Minneap Minn) 2020; 26 (2): pp. 260-267.

2.Ortiz de Mendivil A., et al.: Brainstem stroke: anatomy, clinical and radiological findings . Semin Ultrasound CT MR 2013; 34 (2): pp. 131-141.

3.Silverman I.E., et al.: The crossed paralyses: the original brain-stem syndromes of Millard-Gubler, Foville, Weber, and Raymond-Cestan . Arch Neurol 1995; 52 (6): pp. 635-638.

4.Kim A.S.: Medical management for secondary stroke prevention . Continuum (Minneap Minn) 2020; 26 (2): pp. 435-456.

5.Burger K.M., et al.: Brainstem vascular stroke anatomy . Neuroimaging Clin N Am 2005; 15 (2): pp. 297-324.

6.Pare J.R., Kahn J.H.: Basic neuroanatomy and stroke syndromes . Emerg Med Clin North Am 2012; 30 (3): pp. 601-615.

7.Ovbiagele B., Nguyen-Huynh M.N.: Stroke epidemiology: advancing our understanding of disease mechanism and therapy . Neurotherapeutics 2011; 8 (3): pp. 319-329. PMID: 21691873; PMCID: PMC3250269 .

8.Cramer S.C.: Recovery after stroke . Continuum (Minneap Minn) 2020; 26 (2): pp. 415-434.

Suggested Readings

1. Gorelick P., et al.: Blood pressure management in stroke . Hypertension 2020; 76: pp. 1688-1695.
2. Moncayo J.: Midbrain infarcts and hemorrhages . Front Neurol Neurosci 2012; 30: pp. 158-161.
3. Rabinstein A.A.: Update on treatment of acute ischemic stroke . Continuum (Minneap Minn) 2020; 26 (2): pp. 268-286.
4. Sciacca S., et al.: Midbrain, pons, and medulla: anatomy and syndromes . Radiographics 2019; 39 (4): pp. 1110-1125.
5. Warshaw G., et al.: Ham’s primary care geriatrics . ed 7 2022 . Elsevier , Philadelphia