Strokes, Hemorrhages, and Aneurysms

Strokes

Strokes and TIAs will 100% for sure be on your PANCE/PANRE/PACKRAT/EORs, you name it. While historically, the PANCE and PACKRAT are only 6% Neurology questions, these are a few that you shouldn’t miss. After completing my general neurology rotation, I quickly learned that the answers to these complex puzzles was definitely time-dependent. Can you think on your feet and generate a differential diagnosis? Attention to tiny details was crucial for Neurology because that’s how you can tell what part of the brain the ischemia/infarction is coming from.

I hope this review helps you regardless of which avenue you find it useful. Good luck and make sure to check out TrueLearn’s free sample questions below! The vignette style questions are exactly what you need to prepare yourself for EOR and PANCE related questions. Good luck!

Transient Ischemic Attack, Cerebrovascular Accidents (CVA) or Stroke, Bell’s Palsy

• Evolving stroke: worsening
• Completed stroke: maximal deficit has occurred
• Duration of symptoms is the determining difference
• Transient Ischemic Attacks (TIA)
• Neurologic deficit that lasts few mins to <24 hours (N: 30 mins)
• Symptoms transient because reperfusion occurs due to collateral circulation or breaking up of embolus
• Blockage in blood flow does not last long enough to cause permanent infarction
• Clinical Pearls
• Triptans are contraindicated in patients with coronary artery disease or peripheral vascular disease and should be avoided in all patients with an increased risk for stroke
• Contraindications to thrombolytic therapy: previous hemorrhagic stroke, stroke within 1 year, a known intracranial neoplasm, active internal bleeding, suspected aortic dissection. Relative contraindications: severe uncontrolled hypertension, use of anticoagulation, active peptic ulcer disease.
• Hypertension is the most common and most important stroke risk factor

Ischemic Stroke (85%) Causes in young patients: OCP use, hypercoagulable states (pregnancy, malignancy, vWF, antiphospholipid antibody syndrome), vasoconstrictive drug use (cocaine, amphetamines), polycythemia vera, sickle cell	RF: age and HTN, smoking, DM, hyperlipidemia, atrial fibrillation (cardioembolic), family history of CAD, family history of stroke, previous stroke/TIA, carotid bruits, drugs (sympathomimetics, OCPs, cocaine)	Clinical manifestations See Table 1 Below	1. CT without contrast of head - differentiates ischemic from hemorrhagic (first line), may have to wait 24-48 h to see infarct 2. MRI of brain - more sensitive than CT and identifies ALL infarcts earlier than CT, not preferred in emergent setting 3. EKG - acute MI or A-fib may be cause of embolic strokes 4. Carotid duplex scan - determines degree of stenosis 5. MRA - definitive test for stenosis of vessels of head/neck and for aneurysms	Acute - supportive treatment (airway protection, O2, IV fluids) 1. C-A-B 2. Gradual BP Control - do not give antihypertensives UNLESS SBP >200, DBP >120 or MAP >130 mmHg Preferred: IV Labetalol 20 mg Acute MI, aortic dissection, severe HF, hypertensive encephalopathy Receiving thrombolytic therapy Prevention -Control RF: HTN, DM, smoking, cholesterol, obesity -Aspirin -Carotid endarterectomy -Prevention of lacunar strokes: control HTN Stable 1. t-PA therapy A. If administered within first THREE hours of onset, improved outcome at 3 months B. Do not initiate if: >3 hours, uncontrolled HTN, bleeding disorder or anticoagulated, history of recent trauma or surgery C. Do not give aspirin for first 24 hours if t-PA given, perform frequent neuro checks, carefully monitor BP 2. Aspirin is best if given within 24 hours of symptom onset A. If within 3 hours - give thrombolytics B. If after 3 hours - give aspirin, and if pt allergic, give Clopidogrel → Ticlopidine 3. Anticoagulants (heparin/warfarin) have not been proven to have efficacy in acute stroke 4. Assess patient’s ability to protect airway, keep NPO, elevate HOB to 30 degrees
Embolic Stroke	Most common type MC location: heart (due to embolization of mural thrombus in pt with atrial fibrillation), internal carotid, aorta, paradoxical	1. Onset of symptoms very RAPID (seconds), and deficits are maximal initially 2. Clinical features depend on artery occluded 3. MCA most commonly affected: A. Contralateral hemiparesis (weakness) B. Hemi-Sensory loss C. Hyperreflexia D. Aphasia (90% left) E. Apraxia		High risk of stroke in subsequent months -Risk is 10% per year -30% 5-year risk of stroke
Thrombotic Stroke	Atherosclerotic lesions in large arteries of neck or medium sized arteries of brain (MCA)	1. Onset may be rapid or stepwise 2. Patient awakens from sleep with neurologic deficits
Lacunar Stroke (internal capsule, pons, thalamus) Causes 20% of all strokes; usually affects subcortical structures	Narrowing of large arterial lumen due to thickening of vessel wall (not by thrombosis) RF: history of chronic HTN and DM Affected arteries: MCA, Circle of Willis, basilar and vertebral arteries	Hemiparesis - weakness of entire left or right side 1. Internal capsule: Pure motor hemiparesis 2. Pons: Dysarthria, clumsy hand 3. Thalamus: Pure sensory deficit	Focal features and usually contralateral pure MOTOR or pure SENSORY deficits	-Prevention of lacunar strokes: control HTN
Transient Ischemic Attack	Brief episode of neurologic dysfunction caused by focal brain or retinal ischemia Blockage in flow does not last long enough to cause permanent infarction Retinal artery (MCA) → amaurosis fugax	1. Sudden onset neurologic deficit 2. Lasts minutes to <1 hour (N: 15-30 minutes) 2. Reversal of symptoms within 24 hours	1. Carotid doppler ultrasound   2. MRA of neck	1. Hospital admission for new onset and recurrent TIA, unless confident diagnosis of cause of event can be made 2. Antiplatelet therapy: Aspirin +/- dipyridamole OR Clopidogrel NOTE: If high risk → Warfarin should be used RF for recurrent stroke, average 5% risk per year
Amaurosis Fugax	Etiology: atherosclerosis (emboli to the ophthalmic artery), carotid stenosis	“Fleeting blindness” or “curtain coming down” vertically into field of vision 1. Painless, transient 2. Unilateral (monocular) vision loss 3. Seconds of a graying out of vision in one eye	Retinoscopy: refractile arterial lesions (Hollenhorst plaques, cholesterol crystals)	Annual risk of stroke is 1-2%
Carotid Stenosis	Extracranial internal carotid artery stenosis >80% +/- symptoms of ischemia Asymptomatic - refers to presence of narrowing of the ICA in individuals without a history of recent ipsilateral ischemic stroke or TIA Symptomatic - refers to neurologic symptoms caused by TIA or ischemic stroke in the carotid artery territory and ipsilateral to significant carotid atherosclerotic pathology	Symptoms of ischemia 1. Partial and complete blindness in one eye and absent pupillary light response 2. Contralateral homonymous hemianopsia, hemiparesis, hemisensory loss 3. Left hemisphere - Aphasia 4. Right hemisphere - left visuospatial neglect, constructional apraxia, dysprosody 5. Unilateral limb shaking, transient loss of monocular vision upon exposure to bright light 6. Does NOT cause vertigo, lightheadedness, or syncope Signs 1. Carotid bruit 2. Funduscopic exam: arterial occlusion or ischemic damage to retina	1. Cerebral angiography (gold standard) -Permits use of entire carotid system, provides info about tandem atherosclerotic disease, plaque morphology, and collateral circulation -Identifies people who would benefit from endarterectomy (CEA) 2. Carotid duplex ultrasound -Non-invasive, but hairline residual lumens can be missed and can overestimate degree of stenosis 3. Magnetic resonance angiography (MRA) neck -Less accurate for detecting moderate stenosis, more expensive, time consuming, patient must lie still, renal insufficiency can be an issue 4. CT angiography (CTA) -Impaired renal function is a relative contraindication since contrast bolus must be given (DM/CHF)	See treatment of asymptomatic and symptomatic CAS below
Asymptomatic Bruits 1.Start daily antiplatelet therapy, statin therapy, manage diabetes, treat hypertension, and healthy lifestyle (limit ETOH consumption, weight control, aerobic physical activity, Mediterranean diet) 2. Carotid endarterectomy (CEA): >80% stenosis, recurrent TIAs on medical therapy (preferred) -If patient has life expectancy of >5 years 3. Duplex ultrasonography - repeat annually to assess progression or regression of disease and response to therapeutic intervention if stenosis >50% 4. Carotid artery stenting (CAS) only for high risk patients -Unlikely to benefit if: severe comorbidity, prior ipsilateral stroke, total occlusion of ICA
Symptomatic Bruits - manifested as recent TIA or ischemic stroke and ipsilateral CAS 1. Anticoagulation (Warfarin) 2. Carotid endarterectomy (CEA) indicated for   -Severe stenosis (70-99%) → CEA recommended -Mod stenosis (50-69%) → CEA recommended -Mild stenosis (<50%) → no indication for CEA or carotid angioplasty with stenting -Consider AGE: If >70, CEA may be associated with better outcome compared to CAS; for younger patients, CAS = CEA in terms of periprocedural complications 3. CAS is indicated as an alternative to CEA for symptomatic patients at average or low risk of complications when diameter of lumen of ICA is reduced by >70% by non-invasive imaging, or >50% by catheter angiography, or >50% by noninvasive imaging with corroboration High risk: progression of asymptomatic CAS, detection of embolism, plaque burden and morphology, reduced cerebrovascular reserve, silent embolic infarcts
Bell’s Palsy: hemifacial weakness/paralysis of muscles innervated by CN 7 due to swelling of cranial nerve	Uncertain cause, possibly viral (herpes simplex)	1. URI preceding event 2. Acute onset unilateral facial weakness/paralysis, both UPPER and LOWER parts of face affected 3. Weak orbicularis oculis muscle (cannot raise eyebrows) on affected side Clinical diagnosis --Consider Lyme disease (do not use steroids) --EMG testing if paresis fails to resolve in 10 days	--Usually no treatment required --Short course of prednisone and acyclovir --Wear eye patch to prevent corneal abrasion --Surgical decompression of CN 7	Prognosis good: 80% recover fully within weeks to months

Table 1. Deficits Seen in Ischemic Strokes

Distribution	Location and/or Type of Deficiency
Anterior Cerebral Artery (ACA)	1. Contralateral lower extremity hemiparesis and hemisensory loss (leg > arm) 2. Abulia (especially if bilateral) - inability to make decisions
Middle Cerebral Artery (MCA)	1. Aphasia (if dominant hemisphere involved) - 90% LEFT 2. Agnosia (non-dominant) - inability to process sensory information 2. Apraxia, contralateral body neglect, confusion (if non-dominant hemisphere involved) 3. Contralateral hemiparesis and hemisensory loss 4. Homonymous hemianopsia (variable)
Internal Carotid Artery (ICA)	1. Ipsilateral blindness (variable) 2. MCA syndrome
Vertebral or PICA (posterior inferior cerebellar artery)	1. Ipsilateral: hemiataxia, nystagmus facial sensory loss, Horner syndrome   2. Contralateral loss of temperature or painful sensation 3. Dysphagia
Basilar Artery	1. Quadriparesis 2. Dysarthria 3. Dysphagia 4. Diplopia 5. Somnolence 6. Amnesia
Posterior Cerebral Artery	1. Contralateral homonymous hemianopsia 2. Amnesia 3. Sensory loss
Lacunar (internal capsule, pons, thalamus)	1. Internal capsule: Pure motor hemiparesis 2. Pons: Dysarthria, clumsy hand 3. Thalamus: Pure sensory deficit

• Unfortunately, cocaine use is one of the main causes of stroke in the young
• Common sites of SAH
• Junction of anterior communicating artery & anterior cerebral artery
• Junction of posterior communicating artery & internal carotid
• Bifurcation of the MCA

CHADS2 Scoring

The presence of congestive cardiac failure (C), hypertension (H), age >75 years (A), and diabetes (D) each scores one point, and a history of prior stroke or TIA (S) scores two points. A CHADS score of two or more is associated with an annual risk of stroke of over 4%.

• International treatment recommendations are aspirin 325 mg/day for those with a CHADS score of 0
• For those with a CHADS score of 1, aspirin or warfarin may be used depending on patient preference.
• Patients with a CHADS score of 2 or more should be anticoagulated unless there is a specific contraindication.
• Patients with bacterial endocarditis should not receive warfarin because of the risk of cerebral hemorrhage from septic embolization.

Subarachnoid Hemorrhage or Cerebral Aneurysm, Intracerebral Hemorrhage (ICH)

Hemorrhagic Stroke (15%)
Intracerebral Hemorrhage (ICH): bleeding into the brain parenchyma NOTE: In the acute phase, the mass effect of a cerebral hematoma is far greater than in a large cerebral infarction with a greater risk of herniation and death In chronic phase, prognosis is much better for those with hemorrhage than those with ischemia	Causes: HTN (sudden increase) is most common cause -Ischemic stroke convert to → hemorrhagic stroke Patient develops edema around lesion or expansion of hematoma → herniation of brain tissue Locations: putamen (40%), thalamus, lobar white matter, caudate, pons, cerebellum RF: smoking, advanced age, anticoagulant use	1. Abrupt onset of a focal neurologic deficit worse steadily over 30-90 minutes -Pinpoint pupils - pons -Poorly reactive pupils - thalamus -Dilated pupils - putamen -Decreased level of consciousness 2. Headache, nausea, vomiting - Severity of headache correlates with size of lesion 3. Confusion, aphasia, hypersomnolence Signs 1. Increased ICP 2. Intubated 3. Hypertensive 4. Hyperconvergence, absent vertical gaze, horizontal gaze paresis 5. Sensorimotor: hemiparesis, hemisensory or hemimotor loss, quadriplegia, ataxia 6. Stupor, coma	1. Non-contrast CT scan of head (90% of ICH): hyperintense area with mass effect and (later) hyperintense surrounding edema 2. CT Angiography -Coag panel and platelets -Ophthalmologic examination is mandatory to rule out papilledema	1. Admit, supportive care, control BP a. IV Labetalol, Esmolol, or Nicardipine (Cardene) -Target: SBP <180 -MAP <130 B. Reverse anticoagulants: FFP + Vitamin K, Protamine -Mannitol (osmotic agent) and diuretics to reduce ICP -Steroids harmful, NOT recommended -Rapid surgical evacuation of CEREBELLAR hematomas only 2. Emergent neurosurgery consult High mortality rate (50% at 30 days) 3. Surgery if >3 cm STEROIDS CONTRAINDICATED Complications: increased ICP, seizures, rebleeding, vasospasm, hydrocephalus, SIADH
Cerebral (intracranial) Aneurysm --Develops from normal hemodynamic stress or HTN --Develops at junction of communicating branch with main cerebral artery (Ant Comm + Ant Cerebral) AV malformation	Causes: 1. Ruptured berry (saccular) aneurysm (MCC, 80%) - most located in anterior circulation 2. Fusiform (large) 3. Mycotic (bacterial endocarditis) Associated: polycystic kidney disease, Marfan syndrome	May manifest as compression as cranial nerves (CN 3, 4, 6) Causes of rupture: strenuous activity (exercise, coitus, physical work)	1. Non-contrast CT head - if normal, do LP a. Contrast CT or MRI for aneurysms >5 mm or AV malformations 2. Lumbar puncture 3. Cerebral angiography (gold standard)	1. Open surgical clipping 2. Endovascular coiling (preferred) Complication: Subarachnoid Hemorrhage Of aneurysms that rupture, 33% die before reaching the hospital, 20% die in the hospital, 30% recover without disability
Subarachnoid Hemorrhage (SAH): bleeding into the CSF; outside brain parenchyma	RF: smoking, hypertension, cocaine and alcohol use, first-degree relative with SAH, female, African-American, connective tissue disorders “Thunderclap headache” Locations: saccular aneurysms at bifurcations of arteries of the Circle of Willis	1. Sudden onset severe headache (excruciating) -Absence of focal neurologic deficit -”Worst headache of my life” -Sudden, transient loss of consciousness 2. Nausea, vomiting (common) 3. Neck pain, nuchal rigidity 4. Photophobia, visual changes 5. Decreased level of consciousness (53%) 6. Seizure (20%) Signs 1. Hypertensive 2. Retinal hemorrhage (30%)	1. Fundoscopic exam: retinal hemorrhage 2. Non-contrast CT (first line): negative in 10% → if negative, follow with CSF -Most are negative <2 hours, most sensitive >12 hours 3. Lumbar Puncture -CI: elevated ICP, thrombocytopenia, suspected epidural abscess -Xanthochromia, elevated RBCs 1. Blood in CSF (Hallmark) 2. Xanthochromia (yellow CSF) is gold standard for diagnosis, resulting from RBC lysis by 6 hours 4. CT Angiography 5. Once diagnosed → cerebral angiogram (definitive)	1. Supportive care, admit A. Bed rest in quiet, dark room B. Stool softeners to avoid straining C. Analgesia for headache (tylenol) D. IV fluids for hydration E. Lower BP gradually using CCB (Nifedipine) for vasospasm 2. Craniotomy and clipping - definitive -Coiling: alternative 3. Treat BP aggressively -PO Nimodipine 60 mg should be given x 21 days after to prevent vasospasm High mortality (40-50% at 30 days) Most rebleeding occurs within first 3 days after rupture Complications: rerupture (30%), vasospasm (50%), hydrocephalus, SIADH, hypertension

TrueLearn Questions

Question 1: A 60-year-old woman with a presents to the emergency department because she suddenly “felt her left arm go heavy and numb.” Approximately half an hour prior to arrival at the hospital, she noticed that she could no longer lift her spoon to her mouth. She has not had surgery, head trauma, stroke, or gastrointestinal or urinary bleeding recently. Medications include lisinopril, atorvastatin, metformin, glyburide, nifedipine, aspirin, and clopidogrel. On examination, her temperature is 37ºC (98.6ºF), heart rate is 89 beats/minute, respirations are 18 breaths/minute, and blood pressure is 175/100 mmHg. There is asymmetry of the nasolabial folds and mouth. Pupils are equally round and reactive. There is 2/5 strength in the left upper extremity and 5/5 strength elsewhere. Light touch, pinprick, vibration, and proprioception are markedly diminished in the left upper extremity and intact elsewhere. Head CT shows no evidence of intracranial hemorrhage. Which of the following is true of the use of fibrinolytic therapy in the treatment of this patient?

1. Blood pressure must be reduced to less than 170/100 mm Hg before starting fibrinolytic therapy
2. Fibrinolytic therapy can be given up to 4.5 hours after symptom onset
3. Fibrinolytic therapy is contraindicated because the patient is taking clopidogrel
4. Fibrinolytic therapy is contraindicated in chronic renal failure
5. Fibrinolytic therapy is contraindicated in the setting of recent transient ischemic attack

Explanation:

This patient most likely has suffered an ischemic stroke given her neurologic symptoms. Head CT is negative for intracranial bleed, and her symptoms began 30 minutes prior to arrival to the hospital; therefore, she is a good candidate for thrombolytic therapy. Fibrinolytic therapy can be given up to 4.5 hours after symptom onset or after the patient was last known to be normal, if the time of onset of symptoms is not known. After 4.5 hours mortality associated with fibrinolysis exceeds that associated with stroke. Contraindications to fibrinolytic therapy include: history of intracranial hemorrhage, blood pressure > 185/110 mm Hg, myocardial infarction within three months, major surgery within 14 days, stroke or head trauma within 3 months, INR > 1.7, platelets < 100,000, clearing symptoms, and seizure such that symptoms may be post-ictal rather than due to stroke. If the patient presents within the first 3 hours following onset of symptoms, he/she will receive tissue plasminogen activator (tPA). Between 3 and 4.5 hours, patients can receive recombinant tPA. Additional contraindications to this treatment include age greater than 80, anticoagulation regardless of INR, and history of diabetes.

Answer A: Blood pressure reduction is not a necessary step in preparation for fibrinolytic therapy. This woman's blood pressure is already below the 185/110 mm Hg required for therapy.

Answer C: Use of clopidogrel or other anti-platelet medications is not a contraindication to fibrinolytic therapy; however, use of anticoagulants such as heparin or warfarin is a contraindication.

Answer D: Fibrinolytic therapy is not contraindicated in patients with chronic renal failure.

Answer E: Recent transient ischemic attack (TIA) is not a contraindication to using fibrinolytic therapy. A history of stroke within the last three months, however, is an absolute contraindication.

Bottom Line: Fibrinolytic therapy can be given up to 4.5 hours after symptom onset or after the patient was last known to be normal, if the time of onset of symptoms is not known. For more information, see http://emedicine.medscape.com/article/1160840-overview

Question 2: A 76-year-old male presents to the emergency department with a chief complaint of an inability to move his right upper and lower extremity after waking from a nap an hour ago. A mild aphasia and contralateral facial droop are noted on physical exam. A CT scan (without contrast) of the head reveals dark areas within the middle cerebral artery distribution. During physical examination the patient develops a sudden headache, right pin-point pupil and poor gag reflex with increased respiratory effort. The most appropriate course of action is

1. Administer thrombolytic therapy (t-PA)
2. Immediate intubation
3. Immediate neurosurgical consultation
4. Rapid nitroprusside infusion to reduce blood pressure
5. Repeat stat CT scan without contrast

Explanation:

In the case above the patient presented with an ischemic stroke that converted to a hemorrhagic stroke. In a classic presentation of a thrombotic stroke a patient awakens from sleep with neurologic deficits. Though hypertension is the most common cause of a hemorrhagic stroke, an ischemic stroke may convert to a hemorrhagic stroke. A hemorrhagic stroke presents with headache, vomiting, altered level of consciousness and signs of increased intracranial pressure (ICP). In a patient that displays an altered mental status and respiratory drive, CABs with airway management takes precedence and intubation is frequently required. A head CT scan without contrast is ordered as the first imaging study to differentiate an ischemic from a hemorrhagic stroke. Ischemic strokes appear as dark areas on the CT scan while hemorrhagic strokes appear white.

Answer A: Thrombolytic therapy should not be administered in a patient with a suspected intracranial bleed. t-PA is administered for an acute ischemic stroke within three hours of symptom-onset.

Answer C: Though surgery for hematoma evacuation may be required later, the moreimmediate treatment is airway management

Answer D: Elevated blood pressure increases ICP and can cause further bleeding. BP reduction must be gradual (not rapid) to prevent hypotension which can lower cerebral blood flow and worsen neurological deficits.

Answer E: A repeat CT scan is necessary for the new neurological change. However, more immediate treatment is airway management.

Bottom Line: An ischemic stroke may convert to a hemorrhagic stroke. Any patient with a mental status change and an altered respiratory drive with poor gag reflex requires evaluation of CABs with appropriate airway management. insight: If a patient's airway is compromised, always start with CAB’s first, no matter what the clinical scenario may be.

Question 3: A 61-year-old man with no significant medical history presents to the emergency department after experiencing difficulty speaking at a work holiday party two hours ago. He says that he was talking to a co-worker and suddenly could not find the words to finish the story he was telling. He sat down for a few minutes but finally decided to seek care when he realized that his right hand was weak and his speech had not returned. His symptoms started to resolve shortly before arriving at the emergency department and he says he feels better now but he thinks he is “not quite himself.” His only medicine is a daily multivitamin. On exam he is afebrile, and all vital signs are within normal limits. His speech is somewhat slow and his face is slightly asymmetric. Grip strength in his right hand is 4+/5. No other neurological abnormalities are noted. His cardiac exam shows a regular rate and rhythm with no murmurs, rubs, or gallops. His lungs are clear to auscultation. CT scan shows no abnormalities, and the patient refuses MRI due to claustrophobia. Which of the following is the next best step in the management of this patient?

1. ECG
2. Factor V Leiden screen
3. Lumbar puncture
4. Syphilis serology
5. Transthoracic echocardiography

Explanation:

This patient is exhibiting signs of a transient ischemic attack (TIA). All the tests listed are reasonable in the workup of TIA but evaluation for cardiac arrhythmias as a possible embolic source is the most urgent of the listed options. Bottom Line: TIA needs to be investigated for a cause in order to prevent ischemic stroke in the future. Most patients will require a full cardiac workup in addition to brain imaging.

Question 4: A 45 year-old female with a history of hypertension presents to the emergency department complaining of the worst headache of her life. A CT scan is performed and found to be negative. A lumbar puncture demonstrates xanthochromia. What is the most likely vessel(s) associated with her condition?

1. Posterior cerebral artery and basilar artery junction
2. Posterior cerebral artery and posterior communicating artery junction
3. Anterior communicating artery and anterior cerebral artery junction
4. Middle cerebral artery and internal carotid artery junction
5. Middle meningeal artery

Explanation:

The most likely diagnosis in this patient is a subarachnoid hemorrhage resulting from a ruptured berry aneurysm. The two most common causes of subarachnoid hemorrhage are 1.) ruptured berry aneurysms and 2.) bleeding arteriovenous malformations. Berry aneurysms may develop from normal hemodynamic stresses or in response to hypertension. They usually develop at junctions of communicating branches with their main cerebral arteries. The most common site for a ruptured berry aneurysm is at the junction of the anterior communicating artery and the anterior cerebral artery. When the aneurysm ruptures, blood is released into the subarachnoid space. This blood can be broken down into bilirubin pigments in the CSF which imparts a yellow color to the CSF called xanthochromia. Incorrect: Answer (A): Aneurysms of the posterior cerebral artery and basilar artery junction are responsible for about 4% of subarachnoid hemorrhages due to a ruptured aneurysm. Incorrect: Answer (B): Aneurysms of posterior cerebral artery and posterior communicating artery junction are responsible for about 15% of subarachnoid hemorrhages due to a ruptured aneurysm. Incorrect: Answer (D): Aneurysms of the middle cerebral artery and internal carotid artery junction are responsible for about 20% of subarachnoid hemorrhages due to a ruptured aneurysm. Incorrect: Answer (E): A rupture of the middle meningeal artery leads to an epidural hematoma, not a subarachnoid hemorrhage. Bottom Line: The most common site for a ruptured berry aneurysm is at the junction of the anterior communicating artery and the anterior cerebral artery. Insight: You must know as much as possible about epidural hematomas, subdural hematomas and subarachnoid hemorrhages. You should be able to recognize them based on clinical findings, know how to diagnose them and know how to treat them.