Posterior Circulation Stroke Sunitha Santhakumar, MD The patient is 41 year old male with a past history of alcohol abuse and hypertension who presents to the ED with a chief complaint of loss of balance, slurred speech, and right sided weakness for the past hour and a half. The patient had been out with friends at 8:00 PM, when he fell down suddenly and could not get up or move his right arm and leg. His speech was slurred. He was taken to the ED and arrived at 9:00 PM. On exam, the patient was lying comfortably and in no apparent distress. His BP was 149/79, P 100, RR 18, and T 36.9. His chest, heart, and abdomen were normal and his pupils were R 3.5/L 3.0, reactive, with normal fundi. The patient was alert and oriented x 3 on presentation, later becoming stuporous. He had a left facial droop and gaze palsy to the left. He had R arm and R leg weakness (3/5) and his right side had decreased sensitivity to light touch and pinprick. The patient also had dysmetria on R (not out of proportion to weakness).
Posterior Circulation Stroke Page 2 of 20 Posterior Circulation Stroke Case Details CC: HPI: Loss of Balance The patient is 41 year old male with a past history of alcohol abuse and hypertension who presents to the ED with a chief complaint of loss of balance, slurred speech, and right sided weakness for the past hour and a half. The patient had been out with friends at 8:00 PM, when he fell down suddenly and could not get up or move his right arm and leg. His speech was slurred. He was taken to the ED and arrived at 9:00 PM. PMHx: Alcohol abuse for 12 years, quit 3 years ago Hypertension Seizures, generalized, none in past 7 years MEDS: Hydrochlorthiazide 25mg / triamterene 37.5 mg per day SHx: FHx: Smokes 2 pack per day 15 years Father died of an acute MI, age 62. Mother has Hypertension, NIDDM Review of Systems: Recent URI with nasal congestion, mild nonproductive cough Mild dizzy spells for past 2 weeks, each lasting 5-10 minutes, 2-3 per week Physical Exam: Vitals: BP 149/79, P-100, RR-18, T-36.9 Gen: Patient lying comfortably, in no apparent distress HEENT: Pupils: R 3.5/ L 3.0 reactive. Fundi clear. Chest: Clear to auscultation. Heart: S1, S2 normal, no murmurs. Abdomen: Soft, nontender, no organmegaly Neurologic: Mental status: A& Ox3 on presentation, later became stuporous CN: Dysarthria, pupils: R 3.5/ L 3.0 reactive L facial droop, gaze palsy to the L Motor: R arm and R leg weakness (3/5) Sensory: Decreased to light touch and pinprick on R Coordination: Dysmetria on R (not out of proportion to weakness) NIH Stroke Scale score = 14
Posterior Circulation Stroke Page 3 of 20 Posterior Circulation Stroke Epidemiology Posterior circulation ischemia can range from fluctuating brainstem symptoms, caused by intermittent insufficiency of the posterior circulation (so-called VBI), to the locked-in syndrome," which is caused by basilar artery or bilateral vertebral artery occlusion. Stroke syndromes of the posterior circulation account for approximately 20% of all strokes, with up to 20-60% of patients having an unfavorable outcome. Basilar artery occlusion (BAO) represents 8-14% of all posterior circulation strokes and carries mortality of over 90% 1. However, in the New England Medical Center Registry of Posterior Circulation Strokes, the overall mortality among 407 patients was reported at only 4%, with 79% having minor or no disability 2. Anatomy and Pathophysiology The etiology of posterior circulation ischemia has been thought to be primarily due to local arterial atherosclerosis (large artery disease) and penetrating artery disease (lacunes). However, there is increasing evidence that cardiogenic embolization is more common than previously suspected and is responsible for 20-50% of posterior circulation strokes 2;3. The posterior circulation consists of the vertebral arteries, the basilar artery, the posterior cerebral arteries and their branches 4. These arteries, through short penetrating branches and circumferential branches, supply the brainstem (medulla, pons, and midbrain), the thalamus, the hippocampus, the cerebellum, and parts of the occipital and temporal lobes (including the visual cortex). There is marked variability in the exact arterial anatomy of the posterior circulation. The posterior circulation, unlike the intracranial portions of the anterior circulation, is prone to atherosclerosis much as are other systemic arteries. In the case of one vertebral artery being occluded, collateral flow comes from the opposite vertebral artery, from muscular cervical artery branches, and from posterior communicating artery. The vertebral arteries originate from the subclavian arteries and course through the vertebral foramina of C6-C2, around the atlas, and through the foramen magnum. At the pontomedullary junction both vertebral arteries join to create the basilar artery. The vertebral arteries supply the medulla, the pons, and the cerebellum. The distal vertebral arteries and the basilar artery give rise to the arteries that supply the cerebellum: the superior, anterior, posterior, and inferior cerebellar arteries. The vertebral arteries are prone to atherosclerotic changes at their origin, and at the junction with the basilar artery. The basilar artery and its branches supply the pons and the cerebellum. Distally the basilar artery divides into the posterior cerebral arteries and then the posterior communicating artery in the Circle of Willis. Atherosclerotic lesions can occur anywhere along the trunk of the basilar artery. The posterior cerebral artery (PCA) supplies portions of the midbrain, the thalamus, the hippocampus, the medial temporal lobe, and the occipital lobe, including the visual cortex.
Posterior Circulation Stroke Page 4 of 20 The midbrain contains cranial nerves 3 and 4, the pons contains cranial nerves 5, 6, 7, and 8, and the medulla contains cranial nerves 9, 10, 11, and 12 5. Acute ischemic injury is the result of multiple factors. Vascular obstruction or occlusion is the fundamental disorder leading to hypoperfusion. Irreversible brain damage occurs when the blood flow reduces to below about 20% of normal. Localized cervical compression or a drop in blood pressure may also precipitate focal ischemia. Blood flow may be impaired in the tortuous vertebral arteries, acutely angled branches of the basilar artery, or by atheroma. Hypoxemia, lactic acidosis, and cellular membrane failure result in the excitotoxic cascade that ultimately causes cytotoxic edema (cellular edema) and cellular death. As the blood-brain barrier deteriorates, there is progressive edema, cerebral compression, and later, reactive hyperemia 5;6 Risk Factors The risk factors for posterior circulation strokes are the same as for other forms of cardiovascular disease. These factors may be either uncontrollable risk factors or medical stroke risk factors. The uncontrollable risk factors include age, gender, race, family history of stroke or TIA, or a personal history of diabetes. The medical stroke risk factors include hypertension, heart disease (such as atrial fibrillation or left ventricular hypertrophy), previous stroke or TIA, previous heart surgery, carotid artery disease, peripheral vascular disease, and smoking. Stroke risk doubles with each decade past age 55. African Americans and individuals with a family history of stroke or TIA have a higher risk for stroke. Past history of stroke or a TIA increases the risk of having another stroke up to about ten times. 35% of those who experience TIAs have a stroke within five years. Heart disease like atrial fibrillation increases the stroke risk up to six times. Smoking doubles stroke risk. The most common causes for vertebrobasilar occlusion are atherosclerosis in the elderly, and trauma in the younger population 7. ED Presentation (Signs and Symptoms) Patients may present with a wide variety of syndromes. Neurological dysfunction includes hemi or quadriparesis, cranial nerve deficits (III-XII), respiratory difficulty, altered sensorium, vertigo and ataxia. Multiple cranial nerve signs indicate involvement of more than one brainstem level. Patients may present with only hemiparesis, which may progress rapidly to quadriparesis or a locked-in syndrome. The onset of symptoms may not be as abrupt as with anterior circulation strokes 1;4;5. As the posterior circulation supplies the brainstem, cerebellum, and occipital cortex, the symptoms frequently involve the "5Ds": dizziness, diplopia, dysarthria, dysphagia, and dystaxia. The hallmark of posterior circulation stroke is crossed findings, with cranial findings on the side of the lesion and motor or sensory findings on the opposite side. The exact symptom complex depends on the precise location of the infarct. Some of the common syndromes are described below 5;8. Vertebrobasilar insufficiency (VBI) is a term used to describe fluctuating brainstem symptoms, such as dizziness associated with cranial nerve symptoms or cerebellar dysfunction over a period
Posterior Circulation Stroke Page 5 of 20 of days to weeks. This indicates insufficient flow through the posterior circulation and is essentially a brainstem TIA. Rarely VBI will present as vertigo alone 9. Wallenberg Syndrome or Lateral Medullary Syndrome is characterized by dissociated sensory loss. Vertebral artery and posterior inferior cerebellar artery occlusion causes nystagmus, vertigo, ataxia, hoarseness, dysphagia, Horner's Syndrome and loss of pain and temperature sensation in the face on the same side of the lesion, and loss of pain and temperature on the opposite side of the body. Top of the Basilar Syndrome (Anton Syndrome) is caused by occlusion of the basilar artery tip as it bifurcates into the posterior cerebral arteries thereby affecting the occipital lobes and deeper structures. It results in somnolence, memory defects, confusion, mutism, visual hallucinations, and bilateral loss of vision with unawareness or denial of blindness, as well as vertical gaze paralysis and skew deviation of the eyes. Weber Syndrome is caused by vascular occlusion to the midbrain from an aneurysm or tumor resulting in ipsilateral oculomotor palsy (CN 3 and 4) with contralateral hemiplegia. Dejerine-Roussy Syndrome involves thalamic compromise due to ischemia or malignancy causing a hemisensory loss of all modalities on one side of the body, contralateral to the side of the lesion. Position sense is affected more than any other sensory function, and deep sensory loss is usually more significant than cutaneous sensory loss. The most dreaded posterior circulation infarction is the "Locked-In Syndrome," which is caused by BAO, resulting in bilateral findings due to midbrain infarction 1. The syndrome is characterized by a progression of symptoms leading to quadriplegia with paralysis of horizontal gaze and bilateral facial and oropharyngeal palsy. The patient is awake and is only able to move his or her eyes vertically. This is often preceded by brief brainstem TIAs occurring several times a day. Patients become stuporous or comatose as the reticular activating system becomes involved. TIAs occur for at least 2 weeks prior to posterior circulation stroke presentation in 50% of patients. In a study of 85 cases of angiographically proven basilar artery or bilateral vertebral artery occlusion, prodromal or progressive symptoms occurred in 75% of cases. The most common prodromal symptoms included vertigo, nausea, and headache ranging from days to months before the stroke. Only 5% of patients had isolated vertigo as a prodromal syndrome. In 63% of patients the onset of symptoms was gradual and progressive. The most common presenting symptoms were vertigo, nausea, headache, dysarthria, and cranial nerve palsies. Hemiparesis or tetraparesis was present in 61% of the patients. Thirty-six percent presented awake, while 23% were somnolent and 30% were comatose 8;10;11.
Posterior Circulation Stroke Page 6 of 20 Dizziness / Vertigo Dizziness is a common ED symptom and is often difficult for patients to describe. It can describe symptoms ranging from near-syncope, lightheadedness or faintness to a sensation of movement or dysequilibrium, unsteadiness, or imbalance. The goal of the EM evaluation of patients presenting with dizziness is to obtain an accurate diagnosis and treatment plan. The first challenge is to separate vertigo (the sensation of movement or spinning) from near syncope. If vertigo is identified, a central cause must be distinguished from a peripheral etiology, to avoid misdiagnosing a brainstem stroke or vertebrobasilar insufficiency for the more benign peripheral vertigo. Vertigo alone, without other signs or symptoms, is rarely of central origin, since the brainstem contains a high density of nuclei and tracts. The vestibular, visual, and the proprioceptive systems work together, with a significant amount of redundancy, to maintain spatial orientation. If two of these three systems are incapacitated, there is loss of spatial orientation, but dysfunction or stimulation of any of the three systems can cause dizziness (i.e. visual vertigo from motion pictures, seasickness). The Romberg test eliminates the visual system; therefore, suggesting vestibular or proprioceptive malfunction. These can then be tested independently, to distinguish which of these processes is failing. The sensory end organs of the vestibular system include the semicircular canals and the otoliths. The semicircular canals detect angular acceleration, while the otoliths detect linear acceleration, gravity, and the position of the head in space. These communicate with the vestibular nuclei in the brainstem through the 8 th cranial nerve. The vestibular nuclei communicate with: (1) the extraoccular muscles through CN III, IV, and VI where the vestibulo-occular reflex (VOR) maintains visual field stability during head movements, with nystagmus resulting when efferent signals are unequal or out of balance, (2) the cerebral cortex through connections in the thalamus, with resultant conscious awareness of head position and postural stability, and (3) the cerebellum, which modulates the VOR. The sensory end organs (labyrinths) provide a constant underlying firing frequency. Diseases that cause unequal inputs into the brainstem (such as labrynthitis, benign positional vertigo) create unequal inputs to the cortex and the extraoccular muscles, and produce vertigo and nystagmus. These unequal inputs can undergo central compensation and thereby limit the duration of each episode. In the case of brainstem disease, the compensatory ability is limited and symptoms tend to persist. Persistent symptoms can occasionally be seen in the unusual case of bilateral severe peripheral deficits that may result in permanent vertigo 12;13.
Posterior Circulation Stroke Page 7 of 20 Central Vertigo Peripheral Vertigo Intensity of Vertigo Mild Severe Tinnitus Rare Frequent Associated Cranial Nerve findings Usual None Nystagmus: Visual fixation No inhibition of nystagmus Inhibits nystagmus horizontorotary nystagmus Rare Common Latency (time from head movement to None 3-40 seconds onset of nystagmus) Fatigue None Yes Habituation None Yes Reproducibility Consistent Variable ED Diagnosis and Evaluation Diagnosis is based largely on the history and physical exam. A history of previous drug or medication use, especially alcohol or aminoglycoside exposure, must be explored, since these can be directly toxic to the labyrinths and cause bilateral dysfunction. The physical exam should focus on cranial nerve findings, eye movements (skew deviation) or cerebellar findings combined with opposite long tract (sensory and motor) signs. The Romberg test can point to vestibular dysfunction, and the Nylen-Barany test (also called the tilt test or the Dix Hall-Pike maneuver) can assist in differentiating peripheral from central vertigo. The differential diagnosis of posterior circulation ischemia includes: TIA (VBI), intracerebral hemorrhage, basilar artery aneurysm, metabolic derangement, trauma, tumors, toxic syndromes / drugs, benign positional vertigo, vestibular neuronitis, Meniere s Disease, migraine, seizure, Diagnostic Tools A noncontrast CT scan of the head is the initial study of choice to exclude intracerebral hemorrhage. The limitations of CT scanning for imaging the posterior fossa results from interference from the closely surrounding bone, which produces artifact and limits resolution. MRI is superior to a CT for imaging the posterior fossa, as it is unaffected by bone. While conventional MRI may have limited sensitivity for blood acutely (in the first 2 hours), it provides superior resolution of the brainstem structures. If MRI is available, it is the study of choice for patients with posterior circulation strokes. It can be performed in conjunction with other MR studies, such as MR angiography, diffusion weighted imaging (demonstrates the ischemic core) and perfusion weighted imaging (demonstrates viable but ischemic tissue - the penumbra) 14. Management Therapy for posterior circulation strokes has not been rigorously tested in controlled trials. The TOAST trial 15, the best placebo-controlled randomized trial of low molecular weight heparin, did not demonstrate a benefit in stroke overall. Nonetheless, traditionally heparin has been used
Posterior Circulation Stroke Page 8 of 20 in the treatment of posterior circulation strokes, based upon uncontrolled trials showing benefit compared to historical controls 2. For patients presenting within 3 hours of symptom onset, IV thrombolysis is indicated, providing the patient meets all of the inclusion and exclusion criteria. This therapy is FDA approved for acute stroke, including posterior circulation stroke. The number of posterior circulation strokes in the NINDS trial 16 was small, but there is no indication that response to treatment is different to that of anterior circulation strokes. If t-pa is given, antiplatelet or antithrombotic agents cannot be used for 24 hours. For patients presenting beyond the 3-hour window, conventional antiplatelet and antithrombotic therapy is often used, with wide variation in treatment regimens 2. Some authorities recommend not using a bolus of heparin, while others use a 3000-5000 unit bolus. Infusion rates vary from 600-1000 units per hour. The most common complication of heparin is bleeding, which occurs in 10% of patients. In 2% of patients, bleeding is serious (ICH or requiring transfusion). Intra-arterial thrombolytic therapy has been used successfully for patients with suspected BAO. In a report by Hacke and Zeumer 17, of 65 patients with vertebrobasilar occlusion, 43 received IA therapy with urokinase. Nineteen patients recanalized, with14 patients surviving and 10 patients having favorable outcomes. Those who did not recanalize died. Conventional antiplatelet and antithrombotic therapy was administered to 22 patients, with only 3 surviving. Zeumer 18 further reported on 28 patients with BAO and severe symptoms, who were treated with local intraarterial therapy within 24 hours of symptom onset. Mortality was reduced to 50%, despite severe symptoms at presentation. Gonner 19 reported a similar experience with 10 BAO patients who had severe symptoms. Five had good recovery, associated with complete or partial recanalization, of whom 3 were treated beyond 6 hours of symptom onset. A series of small uncontrolled trials involving over 200 patients demonstrates a 50-100% recanalization rate resulting in a favorable outcome in 25-60% 17-28. In summary, intra-arterial therapy for severe vertebrobasilar syndromes appears to be a reasonable choice given the dismal outcome for these patients. It has not been studied in a randomized fashion, but such studies are underway in Australia.
Posterior Circulation Stroke Page 9 of 20 Posterior Circulation Stroke Conclusion Posterior circulation strokes present with a wide variety of symptoms. Episodes are often staggering and more protracted than those of acute anterior circulation strokes. Patients usually have crossed findings (cranial nerve findings ipsilateral, with motor and sensory findings contralateral) and include some of the 5 Ds (dizziness, diplopia, dysarthria, dysphagia, and dystaxia). In general, patients do well, but those with BAO (or bilateral vertebral artery occlusion) have a grim prognosis, including 90% mortality if they progress to locked-in syndrome or coma. Intravenous thrombolysis is indicated in patients presenting soon enough for treatment initiation within 3 hours of symptom onset. For patients with severe symptoms who are not eligible for intravenous thrombolysis, local or super-selective intra-arterial thrombolysis can be attempted up to 24 hours from symptom onset. Antithrombotic therapy (heparin) is commonly used in clinical practice, based on uncontrolled trials using historical controls. Further study is needed to define the safest and most efficacious treatment modalities for the various types of posterior circulation stroke.
Posterior Circulation Stroke Page 10 of 20 Table 1 Anatomic Region Function Vascular Supply Cerebellum Midbrain Regulation and control of muscle tone, coordination, control of posture and gait Modulation of sensation, movement and consciousness Vertebral artery Posterior inferior cerebellar artery Posterior cerebral artery Clinical Features Syndrome Ipsilateral Contralateral Anetrior vermis Gait, trunk and leg dystaxia Posterior vermis Truncal ataxia Weber 3 rd nerve palsy Hemiplegia- arm & leg Claude 3 rd nerve palsy Cerebellar ataxia, tremor, Benedikt 3 rd nerve palsy Cerebellar ataxia, tremor and corticospinal signs Pons Modulation of sensation, movement and consciousness Basilar artery Parinaud Locked-in syndrome Foville Millard-Gubler Paralysis of upward - gaze and accommodation, fixed pupils Bilateral hemiparesis- arm & leg, facial weakness, lateral gaze weakness, dysarthria Lateral gaze weakness, facial weakness Lateral gaze weakness, facial weakness Hemiparesis- arm & leg - Basilar artery Anterior inferior cerebellar artery Raymond Lateral gaze weakness Hemiparesis- arm & leg Marie-Foix Arm and leg ataxia Hemiparesis- arm & leg Hemisensory loss- pain & temperature Medulla Cerebrum Occipital lobe Infero-medial temporal lobe Thalamus Modulation of sensation, movement and consciousness Visual perception & recognition Visual discrimination Integration of sensory and motor systems Vertebral artery Posterior inferior cerebellar artery Anterior Spinal artery Posterior cerebral artery Posterior cerebral artery Top of Basilar Posterior cerebral artery Wallenberg (Lateral Medullary) Medial Medullary Balint Anton Nystagmus, Vertigo, Ataxia, Sensory loss in face, Hoarseness, Dysphagia, Horner syndrome Weakness and later hemiatrophy of tongue Hemisensory loss- pain and temperature Hemiparesis- arm & leg, Hemisensory loss- touch and proprioception Bilateral loss of voluntary eye movements, poor visual-motor coordination, inability to understand visual objects Bilateral loss of vision, unawareness or denial of blindness Dejerine-Roussy - Hemisensory lossall modalities, hemi-body pain
Posterior Circulation Stroke Page 11 of 20 Posterior Circulation Stroke Reference List 1. Becker KJ: Vertebrobasilar ischemia. [Review] [107 refs]. New Horizons 1997;5:305-315. 2. Caplan L: Posterior circulation ischemia: then, now, and tomorrow. The Thomas Willis Lecture-2000. Stroke 2000;31:2011-2023. 3. Vuilleumier P, Bogousslavsky J, Regli F: Infarction of the lower brainstem. Clinical, aetiological and MRI-topographical correlations. Brain 1995;118:1013-1025. 4. Easton DJ HSMJ, Fauci AS BE, Isselbacher KJ: Cerebrovascular Disease, in AnonymousHarrison's Principle of Internal Medicine. New York, NY, McGraw Hill; 1998:2325-2348. 5. Victor M RAe: Cerebrovascular Disease, in AnonymousAdam's and Victor's Principles of Neurology. New York, NY, McGraw Hill; 2000:821-851. 6. Pulsinelli WA: The ischemic penumbra in stroke. Sci Med 1995;1:16-25. 7. American Heart Association. 2000 Heart and Stroke Statistical Update. 2000. Dallas, TX. (GENERIC) Ref Type: Pamphlet 8. Ferbert A, Bruckmann H, Drummen R: Clinical features of proven basilar artery occlusion. Stroke 1990;21:1135-1142. 9. Gomez CR, Cruz-Flores S, Malkoff MD, Sauer CM, Burch CM: Isolated vertigo as a manifestation of vertebrobasilar ischemia. Neurology 1996;47:94-97. 10. Phan TG, Wijdicks EF: Intra-arterial thrombolysis for vertebrobasilar circulation ischemia. [Review] [55 refs]. Critical Care Clinics 1901;15:719-742. 11. Castillo M, Falcone S, Naidich TP, Bowen B, Quencer RM: Imaging in acute basilar artery thrombosis. Neuroradiology 1994;36:426-429. 12. Daroff RB MJFABEIK: Faintness, Syncope, Dizziness, and Vertigo, in Anonymous Harrison's Principle of Internal Medicine. New York, NY, McGraw Hill; 1998:100-107. 13. Olshaker JS RPBR: Vertigo, in Emergency Medicine, Concepts and Clinical Practice. St. Louis, MO, Mosby; 1998:2165-2173.
Posterior Circulation Stroke Page 12 of 20 14. Culebras A, Kase CS, Masdeu JC, et al: Practice guidelines for the use of imaging in transient ischemic attacks and acute stroke. A report of the Stroke Council, American Heart Association. Stroke 1997;28:1480-1497. 15. Low molecular weight heparinoid, ORG 10172 (danaparoid), and outcome after acute ischemic stroke: a randomized controlled trial. The Publications Committee for the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) Investigators. [see comments]. JAMA 1998;279:1265-1272. 16. The National Institute of Neurologic Disorders and Stroke rt-pa Stroke Study Group. Tissue Plasminogen Activator for Acute Ischemic Stroke;. New England Journal of Medicine 1995;333:1588-1593. 17. Hacke W, Zeumer H, Ferbert A, Bruckmann H, del Zoppo GJ: Intra-arterial thrombolytic therapy improves outcome in patients with acute vertebrobasilar occlusive disease. Stroke 1988;19:1216-1222. 18. Zeumer H, Freitag HJ, Zanella F, Thie A, Arning C: Local intra-arterial fibrinolytic therapy in patients with stroke: urokinase versus recombinant tissue plasminogen activator (r-tpa). Neuroradiology 1993;35:159-162. 19. Gonner F, Remonda L, Mattle H, et al: Local intra-arterial thrombolysis in acute ischemic stroke. Stroke 1998;29:1894-1900. 20. Sasaki O, Takeuchi S, Koike T, Koizumi T, Tanaka R: Fibrinolytic therapy for acute embolic stroke: intravenous, intracarotid, and intra-arterial local approaches. Neurosurgery 1995;36:246-252. 21. Egan R, Clark W, Lutsep H, Nesbit G, Barnwell S, Kellogg J.: Efficacy of Intra-arterial Thrombolysis of Basilar Artery Stroke. J Stroke Cereb Vas Dis 1999;8:22-27. 22. Thyagarajan D, Stark RJ, Frayne J, Gilligan BS, Sacharias N: Thrombolytic therapy in vertebrobasilar occlusion. Clinical & Experimental Neurology 1992;29:129-142. 23. Cross DT, Moran CJ, Akins PT, Angtuaco EE, Diringer MN: Relationship between clot location and outcome after basilar artery thrombolysis. Ajnr: American Journal of Neuroradiology 1997;18:1221-1228. 24. Becker KJ, Monsein LH, Ulatowski J, Mirski M, Williams M, Hanley DF: Intraarterial thrombolysis in vertebrobasilar occlusion. Ajnr: American Journal of Neuroradiology 1996;17:255-262. 25. Wijdicks EF, Nichols DA, Thielen KR, et al: Intra-arterial thrombolysis in acute basilar artery thromboembolism: the initial Mayo Clinic experience. [Review] [13 refs]. Mayo Clinic Proceedings 1997;72:1005-1013.
Posterior Circulation Stroke Page 13 of 20 26. Brandt T, von Kummer R, Muller-Kuppers M, Hacke W: Thrombolytic therapy of acute basilar artery occlusion. Variables affecting recanalization and outcome. Stroke 1996;27:875-881. 27. Huemer M, Niederwieser V, Ladurner G: Thrombolytic treatment for acute occlusion of the basilar artery. Journal of Neurology, Neurosurgery & Psychiatry 1995;58:227-228. 28. Casto L, Caverni L, Camerlingo M, et al: Intra-arterial thrombolysis in acute ischaemic stroke: experience with a superselective catheter embedded in the clot. Journal of Neurology, Neurosurgery & Psychiatry 1996;60:667-670.
Posterior Circulation Stroke Page 14 of 20 Posterior Circulation Stroke Case Outcome The patient s mental status deteriorated, with a repeat NIHSS score of 22. He received intravenous thrombolysis (t-pa) within 3 hours of symptom onset. He had significant early improvement, but without complete resolution of symptoms. On day 4, the NIHSS score was 10. On his MRA, the L superior cerebellar artery and R&L Ant-Inferior cerebellar arteries were non-visualized. The presumed etiology of the infarct was atherosclerotic vascular disease. Cardiac evaluation was negative. He was discharged on Coumadin to In-patient Rehabilitation.
Posterior Circulation Stroke Page 15 of 20 Posterior Circulation Stroke Suggested Reading 1. Kyra J. Becker. Vertebrobasilar Ischemia. New Horizons 1997; 5:305-315): An excellent review of the presentation, physical findings and therapy of acute vertebrobasilar syndromes. 2. Caplan L.Posterior circulation ischemia: then, now, and tomorrow. The Thomas Willis Lecture-2000.Stroke. 2000 Aug;31(8):2011-23. This manuscript was presented by Louis Caplan as the annual Willis Lecture at the American Stroke Association s International Stroke Conference 2000. It provides an excellent review of the history of vertebrobasilar stroke and discusses the myths versus the data of the natural history of the disease. It reviews the underlying data for current therapy and future therapeutic directions. 3. Easton DJ, Hauser SL, Martin JB. Cerebrovascular Disease, Chapter 366. In: Fauci AS, Braunwald E, Isselbacher KJ, et al eds: Harrison s Principle of Internal Medicine, 14 th Edition, New York, NY: McGraw Hill 1998: 2325-2348. This textbook chapter lays the foundation for the initial evaluation of posterior circulation strokes. It also reviews the various stroke syndromes. 4. Ferbert A, Bruckmann, Drummen R. Clinical Features of Proven Basilar Artery Occlusion. Stroke 1990; 21:1135-1142. An excellent article reporting a large series of patients with clinical and anatomic (angiographic) correlation of basilar artery thrombosis. It reports a wide variation in individual anatomy. It also relates the prodromal syndromes to the clinical course. 5. Olshaker JS. Vertigo, Chapter 127. In: Rosen P, Barkin R, eds. Emergency Medicine, Concepts and Clinical Practice, 4 th edition. St. Louis, MO. Mosby 1998; 2165-2173. This chapter in Rosen s textbook of Emergency Medicine provides an unusually clear explanation of the physiology of vertigo. It contains a practical clinical approach to the patient with acute vertigo with the focus of separating peripheral from central causes of vertigo
Posterior Circulation Stroke Page 16 of 21 6. Thanh G. Phan and Eelco F. M. Wijdicks. Intra-arterial thrombolysis for vertebrobasilar circulation ischemia. Critical Care Clinics Oct. 1999; 15:719-742. This review documents the various smaller studies in intra-arterial therapy for vertebrobasilar ischemia. They are well tabulated and indicate a need for a large randomized trial of intra-arterial therapy. As the prognosis for untreated basilar artery occlusion is so poor, a randomized trial may difficult to carry out. 7. www.strokecenter.org, The Internet Stroke Center at Washington University, St. Louis, MO. This web site is an extensive collection of information on all types of stroke for both the lay public and the professional. Career stroke investigators commonly use it to stay abreast of developments, important articles, and as an extensive bibliography that is easily accessed. 8. www.strokeassociation.org, American Stroke Association, a division of the American Heart Association. The AHA web site on stroke reviews is geared for both laypersons and professionals. It has demographic data, incidence, cost analysis, and a review of risk factors for both cardiovascular disease and stroke. 9. www.stroke.org, The National Stroke Association. The NSA web site is very similar to the AHA web site and serves as an excellent resource to confirm data. The NSA also provides certification in the NIH Stroke Scale
Posterior Circulation Stroke Page 17 of 20 Posterior Circulation Stroke Questions 1. All of the following are posterior circulation syndromes except: a. Ipsilateral CN III palsy with contralateral hemiplegia b. Ipsilateral facial palsy with contralateral hemiplegia c. Hemiplegia and hemisensory loss of the face, arm and leg on one side of the body d. Ipsilateral ataxia and Horner s with contralateral loss of pain and temperature sensation 2. Locked-in Syndrome consists of: a. Coma with quadriplegia b. Bilateral upper extremity weakness greater than lower extremity weakness c. Quadriplegia, bilateral facial and oropharyngeal palsy but preservation of cortical function and vertical gaze d. Cranial nerve findings contralateral to motor and sensory findings 3. Vertigo of central origin is: a. Generally severe and sudden in onset b. A very common isolated prodromal symptom of VBI c. Often associated with tinnitus d. Fatigues easily e. Generally associated with cranial nerve findings 4. Proven therapy for posterior circulation stroke includes: a. Heparin b. Low molecular weight heparin c. IV thrombolysis d. Intra-arterial regional thrombolysis e. Intra-arterial local thrombolysis 5. Overall mortality for posterior circulation strokes is: a. < 5% b. 20% c. 40% d. 70% e. 90%
Posterior Circulation Stroke Page 18 of 20 6. Mortality for Locked-in Syndrome is: a. < 5% b. 20% c. 40% d. 60% e. 80%
Posterior Circulation Stroke Page 19 of 20 Posterior Circulation Stroke Answers 1. Answer c. The hallmark of posterior circulation stroke is that of crossed findings; with cranial findings on the side of the lesion and motor or sensory findings on the opposite side. 2. Answer c. Bilateral ventral pons lesions may result in preserved consciousness and sensation due to sparing of the reticular formation, but paralysis of all movements except vertical gaze and eyelid opening. Bilateral corticospinal and corticobulbar tracts are involved causing quadriplegia, dysarthria, aphonia and weakness of entire side of face. Bilateral involvement of fascicles of CN VI leads to inability to move eyes horizontally. 3. Answer d. Vertigo of central origin is generally mild in intensity. There will be other neurologic findings like multiple cranial nerve, brainstem tract signs and cerebellar ataxia. Patients are ataxic with their eyes open. Coarse horizontal and vertical nystagmus is usually seen. Tinnitus is rare. Hearing is normal. 4. Answer c. In 1995, the National Institute of Neurological Disease and Stroke (NINDS) thrombolysis trial demonstrated a significant improvement in the 90 days outcome in the patients treated with intravenous t-pa within 3 hours of stroke onset. The majority of patients in this trial were anterior circulation strokes, even though posterior circulation strokes were included in the trial. A subgroup analysis of these posterior circulation strokes has not been done. This therapy is FDA approved for clinical use in all types of ischemic stroke. A randomized trial of intra-arterial therapy for BAO is underway. 5. Answer a. Overall mortality of posterior circulation strokes is 4% according to the New England Medical Center Registry on posterior circulation strokes.
Posterior Circulation Stroke Page 20 of 20 6. Answer e. Mortality for Locked-in Syndrome is >80%. The patients are mute and quadriparetic but conscious. The basilar insufficiency should be recognized before the patient reaches this stage. Early symptoms and signs, in the form of TIAs occur in about 50% of the patients for at least 2 weeks prior to presentation.