Vertebral Artery Compression of the Medulla

ORIGINAL CONTRIBUTION Vertebral Artery Compression of the Medulla

Sean I. Savitz, MD; Michael Ronthal, MD; Louis R. Caplan, MD

Background: Intracranial arteries in the subarachnoid Results: We found that compression most commonly oc- space may compress the brain parenchyma and cranial curs at the ventrolateral surface. The clinical features can nerves. Most arterial compressive lesions have been attrib- be transient or permanent and are predominantly motor uted to dolichoectasia in the vertebral-basilar system, and and cerebellar or vestibular, but a poor correlation exists prior reports have concentrated on the pressure effects of between the clinical findings and the severity or extent of basilar artery ectasia. Much less is known about vertebral impingement. The vertebral arteries were angulated, tor- artery compression of the medulla. tuous, or dilated but not necessarily dolichoectatic to cause obvious indentation. Seven patients were treated with an- Objective: To describe a series of patients with verte- tiplatelets and anticoagulants or analgesics, whereas 2 un- bral arteries compressing the medulla oblongata. derwent microvascular decompression, resulting in temporary or no relief. One surgical patient developed cranial Design: Prospective case studies. nerve complications. Among the medically treated patients, none had progression of deficits, and those with single Setting: Tertiary care center. episodes had no recurrence of symptoms. Conclusion: This study is the largest collection, to our Patients: Nine symptomatic patients, 4 men and 5 knowledge, of patients with medullary vascular com- women, between the ages of 32 and 79 years. pression. Further studies are needed to estimate its fre- quency, natural course, and preferred management. Main Outcome Measures: Clinical phenomena, radiographic findings, treatment, and outcomes. Arch Neurol. 2006;63:234-241

EREBRAL ARTERIES IN THE ated by at least 1 of the authors, including clini- subarachnoid space may cal phenomena, radiographic findings, treat- generate pressure and dis- ment, and outcome. All patients underwent tortion of the brain paren- magnetic resonance imaging (MRI) and mag- chyma and stretching of netic resonance angiography. The main inclu- sion criterion was obvious medullary compres- theC cranial nerves. Most intracranial arte- sion by a vertebral artery, which was ectatic, rial compressive lesions have been attrib- tortuous, or dilated. Patients were excluded if uted to dolichoectasia, which refers to di- they had dolichoectasia of the basilar artery or lation, enlargement, and tortuosity of if they had other brain or vascular imaging find- vessels.1 Within the cervicocranial arter- ings that better explained their symptoms and ies, dilatative arteriopathy preferentially in- signs. None of the patients had vascular occlu- volves the vertebrobasilar system. Past re- sive lesions above the vertebral arteries in the pos- ports have emphasized basilar artery ectasia terior or anterior circulation. compressing the pons and cranial nerves exiting the pons, causing trigeminal neural- RESULTS gia and hemifacial spasm2-4 and also caus- 3,5 6,7 ing pontine infarcts. Other reports have DEMOGRAPHICS described the general features and clinical symptoms of vertebrobasilar dolichoecta- The clinical characteristics of the 9 pa- sia. Compression of the medulla by dilated tients are summarized in Table 1. There and/or tortuous vertebral arteries is less well were 4 men and 5 women. Ages ranged from known. We report herein a series of pa- 32 to 79 years. There was a bimodal age dis- tients with vertebral arteries compressing the tribution at initial symptom presentation. medulla oblongata. Four patients developed their first symp- Author Affiliations: toms in their 30s, and 5 patients first pre- Department of Neurology, METHODS sented at older than 60 years. There were 8 Beth Israel Deaconess Medical white individuals and 1 African American Center, Harvard Medical From 1998 to 2004, we prospectively collected individual. None of the patients had large School, Boston, Mass. information on 9 symptomatic patients evalu- artery occlusive lesions.

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Patient No./ Sex/Age, y Medical Conditions Symptoms Neurologic Examination Result Location of Medullary Compression 1/M/71 Hypertension Tinnitus Normal Left lateral surface and pyramid 2/M/79 Hypertension Left leg weakness for 5 min Normal Left lateral surface and pyramid 3/F/35 None Throbbing headaches Normal Tortuous artery indenting on lateral surface and pyramid 4/M/68 Hypertension Sudden 20-s imbalance, Normal Left lateral surface, base, and pyramid veering to the right 5/F/63 Hypertension, DM Sudden left leg tingling Left hemiparesis Right lateral surface, base, and gradual weakness of left and adjacent T2 hyperintensity arm and leg for 3 wk in right medial medulla 6/F/34 None Multiple episodes of Normal Tortuous left vertebral compression unsteadiness, aural fullness, on left side at the base tinnitus, nausea, headache and tegmenta-basal junction 7/F/32 None Hoarseness and dysphagia Vocal cord paralysis, asymmetric S-shaped left vertebral pressing on left lateral left palate elevation surface at middle aspect, sparing pyramids 8/F/63 Hypertension Left arm tingling and left leg Left limb hyperreflexia Left lateral and basilar surface weakness for 2 d 9/F/32 None Episodes of headache, vertigo, LOC Torsional nystagmus to the left, Tortuous, dilated left vertebral compression reduced left corneal reflex on left middle basilar part and pyramid

Abbreviations: DM, diabetes mellitus; LOC, loss of consciousness.

CLINICAL PHENOTYPES

The symptoms and signs of each patient at initial evaluation are summarized in Table 1. Three patients had a single episode of symptoms that did not recur, 4 patients had multiple recurrent episodes, and 2 patients sus- tained permanent deficits. Three patients presented with motor limb weakness, 2 ipsilateral and 1 contralateral to the side of compression; 3 patients had vertigo or gait ataxia; 1 patient had hoarseness, vocal cord paralysis, and abnormal palate elevation ipsilateral to the side of compression; 1 patient had isolated tinnitus; and 1 patient had only throbbing headaches.

BRAIN IMAGING

Both MRI and magnetic resonance angiography were performed in all 9 patients. The findings are summarized alongside the clinical features in Table 1. Com- pression was present mostly along the lateral surface and involved the pyramids in all patients but the tegmentum in only 1 patient (Figures 1, 2, 3, 4, 5, and 6). All except 1 patient had compression by the left vertebral artery, indenting on the left surface of the Figure 1. A 79-year-old man suddenly developed left leg weakness while medulla. Only 1 patient (patient 5; Figure 4) had a walking. He leaned on a family member for support until the weakness right vertebral artery that compressed the right medul- resolved 5 minutes after onset. Magnetic resonance imaging showed a left lary surface. This patient also had increased signal on vertebral artery pressing on the anterolateral left surface of the medulla. T2-weighted imaging studies within the right medial medulla, representing either wallerian degeneration or damage from branch artery occlusion or compression hoarseness but developed cranial nerve complications and (Figure 4C). Of note, 3 patients had MRIs that showed occipital neuralgia. Patient 9 had temporary relief of symp- enlarged cisterns (Figures 3, 5, and 6). toms, but episodes recurred 4 months after surgery. The 3 patients with single transient episodes treated conser- TREATMENT AND CLINICAL COURSE vatively have not had recurrences to date.

Six patients were treated conservatively with analgesics, REPORT OF CASES antiplatelets, and anticoagulants, whereas 2 patients had decompressive surgery (patients 7 and 9 in Table 2). We describe 2 patients to illustrate different clinical Patient 7 had slight postoperative improvement of her features.

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Figure 2. A 35-year-old woman developed throbbing headaches, although the results of a neurologic examination were normal. Magnetic resonance imaging showed impingement of the left anterolateral surface (A) by an angulated left vertebral artery (B).

A B

Figure 3. A 68-year-old man developed sudden onset of ataxia, veering to the right, and vertigo for 20 seconds. Magnetic resonance imaging showed severe indentation (A) and displacement to the right of the medulla (B).

Patient 4 approximately 20 seconds and did not recur. His neurologic examination results were normal. An MRI was ob- A 58-year-old man with hypertension suddenly lost his tained the following day (Figure 3), which showed an ec- balance while standing near his desk at work and felt his tatic left vertebral artery severely compressing the antero- body suddenly being directed to the right. He sensed that lateral medulla. The MRI showed no acute infarcts on the ground was moving underneath him. The episode lasted diffusion-weighted imaging and no hemorrhages on sus-

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Figure 4. A 63-year-old man developed gradual left-sided weakness throughout 3 weeks and then improved during the next 2 months. Magnetic resonance imaging showed compression of the right anterolateral surface of the medulla (A) by an angulated right vertebral artery (B) with resulting T2 hyperintensity in the right medial medulla (C).

ceptibility scans. The T2-weighted imaging results were normal. He was prescribed warfarin sodium and has had no further episodes.

Patient 5 A 63-year-old man with hypertension and diabetes felt a prickling sensation in his left leg. An hour later, he had dif- ficulty controlling this leg and the left hand. Results of a computed tomogram of the head that day and 2 days later were normal. While in Turkey during the next 3 weeks, his arm and leg became progressively weaker to the point where he could not move his hand or push down on the clutch pedal of his car. There was no involvement of his face. The weakness then stabilized and slowly improved during the next 2 months, after which he was examined (L.R.C.). On neurologic examination, no cranial nerve ab- normalities were apparent. Fine finger movements were slow using the left hand, but his proximal strength was normal. There was a left foot drop and weakness of the ham- strings and anterior tibialis with brisk reflexes and a left extensor plantar response. An MRI showed a tortuous right vertebral artery compressing the anterolateral medulla, par- ticularly at its basal portion near the pyramidal tract, and an increased T2 signal in the pyramid itself (Figure 4A-C). The vertebral artery was patent. He was prescribed aspirin and a generous fluid regimen. Two years later, he was walking several hours per day with a short leg brace and had Figure 5. A 63-year-old woman developed sudden onset of left hemiparesis and only slight weakness of the leg extensors. hemisensory loss. Both symptoms resolved after 2 days. Magnetic resonance imaging showed medullary compression along the left anterolateral surface.

COMMENT CLINICAL AND RADIOLOGIC FEATURES Medullary compression by the vertebral artery is a little- known clinical entity in the medical literature. There are In our series, the clinical symptoms were variable but mostly 14 prior case reports, totaling 19 patients8-21 (Table 3). consisted of motor and cerebellar or vestibular symptoms We now describe the largest series, to our knowledge, of and signs. Compression typically occurred along the an- patients with this condition. From this collection, the ma- terolateral surface, consistent with prior reports (Table 3). jor findings were as follows: patients can present with tran- The lateral segments of the medulla contain the cortico- sient symptoms or permanent deficits, motor and vestibu- spinal tracts, which when damaged can cause either con- lar or cerebellar features are the most common clinical pre- tralateral or ipsilateral findings depending on the rostral- sentations, there is a poor correlation between radiographic caudal location of the compression. Two of our patients features and symptoms, and surgery may provide only tem- with hemiparesis had ipsilateral findings, and 1 patient had porary symptom relief and cause other complications. contralateral findings. In the lateral corticospinal tract, the

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Figure 6. A 32-year-old woman had multiple recurrent episodes of vertigo, throbbing headache, and passing out when she stood. Magnetic resonance imaging showed a dilated left vertebral artery impinging and indenting on the anterolateral left surface of the medulla (A and B). She underwent microvascular decompression with temporary relief of all symptoms for 4 months.

could explain the vocal cord paralysis in patient 7 and dys- Table 2. Management and Subsequent Clinical Course phagia and dysphonia seen in previously described patients.14,21 Aural symptoms may be explained by impinge- Patient ment on the cochlear nuclei or the eighth cranial nerve No. Therapy Follow-up exiting the medulla. Bulbar compression has also been sug- 1 Aspirin Tinnitus persists gested as a possible cause of refractory hypertension22,23 and 2 Aspirin and No episodes in 1 year 10 dipyridamole sleep-disordered breathing, but we did not see these fea- 3 Analgesics Headaches responsive tures in any of our patients. to analgesics In some of our patients, the clinical features did not 4 Warfarin sodium No episodes in 1 year match the radiographic findings. In particular, patients with 5 Aspirin Significant improvement at 3 years; transient symptoms such as ataxia or limb weakness had uses a leg brace severe medullary compression (Figure 3 and Figure 5) and 6 Aspirin No further deficits at 1 year 7 Decompression After surgery, hoarseness improved; yet no significant deficits. Patients who had nausea and ver- occipital neuralgia, left ear deafness, tigo did not show compression of the dorsolateral me- oscillopsia, vertigo, and weak tongue dulla or periventricular nuclei such as the area postrema. 8 Aspirin No further episodes in 4 years However, the possibility exists that ventrolateral impinge- 9 Decompression Episodes disappeared for 4 months, ment could lead to distortion of the dorsolateral areas. Seven then recurred; magnetic resonance imaging showed displacement of 9 patients had MRIs that showed pyramidal tract in- of left tegmentum and base volvement at the ventral surface of the medulla, and only 2 patients had pyramidal signs on examination. Overall, we found a poor correlation between symptoms and signs and the extent and severity of compression. fibers innervating the lower extremities are located later- ally. In patients with transient leg weakness, the clinical VESSEL DISEASE features correspond to the topographic distribution of these fibers (Figure 1). Neighboring tracts, such as the spino- The intracranial posterior circulation arteries often show thalamic and spinocerebellar pathways, did not appear to regions of dolichoectasia, which can stretch cranial nerves, be involved in our patients, but hypoalgesia and hypo- compress the brainstem, and cause brain infarcts.6 How- thermesthesia were reported in 1 patient with vertebral ar- ever, in our series, we found that the vertebral arteries tery lateral medullary compression.20 Anterolateral com- were sometimes tortuous, angulated, and/or dominant pression of the lower cranial nerves or the nucleus ambiguus but not necessarily elongated and dilated (Figure 2B).

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Patient Age, y/ Sex Radiographic Findings Clinical Findings Treatment Outcome Reference 53/M Left tortuous VA pressing Progressive left hemiparesis MVD Improvement 8 on lateral surface and left cranial nerve XII 30/M Left elongated VA crossed Quadriparesis and bilateral MVD Slight improvement 9 ventral surface sensory loss after 1 month, then progression 5/M Left VA loop compressing Central sleep apnea Acetazolamide No change 10 ventral surface 38/M Right VA loop compressing Torticollis, vertigo, vomiting, MVD Cervical stiffness improved 11 cervicomedullary arrhythmias junction/cranial nerve XI 30/M Elongated left VA Progressive hemiparesis MVD No change; sectioning of VA 12 led to improvement in weakness 56/M Ectatic left VA compressing Gradual left hemiparesis None Not reported 13 ventral cervicomedullary junction 36/M Tortuous right VA Progressive right hemiparesis MVD Gradual improvement on ventrolateral surface and hypoalgesia, dysphagia 14 47/M Tortuous left VA Left ear deaf, gait ataxia MVD Ataxia improved on ventrolateral surface of pontomedullary junction 54/F Left lateral surface Hypertension, hyperekplexia, 1 Patient: MVD Blood pressure normalized, 15 74/F hemiparesis startle responses disappeared 47/M Left ectatic VA compressing Palatal myoclonus MVD Cured 16 inferior olive 51/M Bilateral VA compression Left hemiparesis MVD of Relief of symptoms 17 of ventrolateral surface and hemisensory loss both arteries 53/F Elongated and curved Right hemiparesis MVD Gradual improvement 18 left VA pressing and hemihypesthesia ventrolateral surface 70/M Left dolichoectatic VA pressing Rapid progression MVD Respirations normalized; 19 on cervicomedullary region of cranial nerves III-XII, cranial nerves III, VI, VII, and VIII quadriparesis, titubation, resolved in 6 months; respiratory distress quadriparesis persisted 54/M Right ectatic VA Left hypoalgesia None Slight improvement 20 on lateral surface and hypothermesthesia 63/M Ectatic VAs Dysphagia (3), dysphonia (1), MVD (5) 4 Patients almost asymptomatic, 21 58/M hemiparesis (1), 1 patient with slight improvement 55/F quadriparesis (3) 67/M 73/M

Abbreviations: MVD, microvascular decompression; VA, vertebral artery.

Dolichoectasia is therefore not required for the verte- explain why in some patients, the clinical symptoms bral artery to impinge on the medulla. Several factors likely did not match the location of medullary compression, contribute to the anatomical variations. We found that similar to an expanding extraparenchymatous mass most of our elderly patients had hypertension and dia- lesion such as a subdural hematoma or congenital betes, which may cause progressive vascular wall dam- anomaly such as Arnold-Chiari malformation. Com- age. Younger patients may have genetic predispositions. pression may be gradual, allowing for adaptation, For example, dolichoectasia occurs in young patients with which may reduce the risk of damaging respiratory Marfan syndrome, acquired immunodeficiency syn- and autonomic centers in the medulla. drome, sickle cell disease, and Fabry disease.24,25 The Another potential mechanism is ischemic injury. young patients in our study (patients 3, 6, 7, and 9) had Compression could generate pressure on perforating negative evaluation results for these conditions. branches from the vertebral artery. Traction on these arteries could disrupt blood flow and cause small- MECHANISMS OF BRAIN INJURY vessel infarcts or migrainelike headaches, as seen in patient 3. Elongation and angulation of the intracra- Vertebral arteriopathies cause neurologic symptoms nial arteries can stretch and distort the orifices of arte- through multiple mechanisms. Direct medullary com- rial branches. Dilatative arteriopathy, for example, can pression is the likely cause for certain patients with lead to decreased blood flow in penetrating branches gradual and persistent symptoms. External compres- of the basilar artery and cause pontine infarcts.5,26 sion of brain structures often causes symptoms away Transcranial Doppler studies of patients with dolicho- from the local region of compression. This may ectasia have shown abnormal flow patterns. Blood

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©2006 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/01/2021 flow is often to and fro within the dilated artery, caus- quency of medullary vascular compression, its natural ing reduced antegrade flow in the vertebrobasilar sys- history, and its preferred treatment. tem.6,27 Blood flow insufficiency under these circum- stances can lead to transient ischemic attacks and Accepted for Publication: September 27, 2005. therefore may be the cause of the transient symptoms Correspondence: Sean I. Savitz, MD, Department of Neu- seen in some of our patients. Reduced flow can also rology, Beth Israel Deaconess Medical Center, Harvard lead to thrombus formation within the dilated seg- Medical School, Boston, MA 02215 (ssavitz@bidmc ments, obstruction of penetrating branches by the .harvard.edu). thrombus, or embolization of clot fragments into the 28 Author Contributions: Study concept and design: Savitz, small-vessel perforators. Alternatively, atheroscle- Ronthal, and Caplan. Acquisition of data: Savitz and rotic plaques may form along the dilated vessel wall Caplan. Analysis and interpretation of data: Savitz and and obstruct the arterial branches. Caplan. Drafting of the manuscript: Savitz and Caplan. Patient 5 had an angulated right vertebral artery Critical revision of the manuscript for important intellec- (Figure 4B) pressing on the lateral surface of the me- tual content: Savitz, Ronthal, and Caplan. Administra- dulla (Figure 4A), and MRI showed a T2 hyperintensity tive, technical, and material support: Savitz and Ronthal. in the medial medulla (Figure 4C). Although the lesion Study supervision: Ronthal and Caplan. could represent an infarct, a 3-week history of progres- Funding/Support: This work was supported in part by sive symptoms is atypical for the development of a stroke. the Fellow to Faculty Transition Award (Dr Savitz) from The lesion could represent either an unusual “slow stroke” the American Heart Association, Dallas, Tex. mediated by altered flow in a branch of the vertebral artery or wallerian degeneration. REFERENCES TREATMENT AND OUTCOME 1. Caplan LR. Dilatative arteriopathy (dolichoectasia): what is known and not known. Ann Neurol. 2005;57:469-471. The best treatment of patients with bulbar compression 2. Boeri R, Passerini A. The megadolichobasilar anomaly. J Neurol Sci. 1964;11: by a vertebral artery is unknown. In all prior reports ex- 475-484. cept for 3, the patients were treated surgically (Table 3). 3. Nishizaki T, Tamaki N, Takeda N, Shirakuni T, Kondoh T, Matsumoto S. 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