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Original Contribution |

Vertebral Artery Compression of the Medulla FREE

Sean I. Savitz, MD; Michael Ronthal, MD; Louis R. Caplan, MD
[+] Author Affiliations

Author Affiliations: Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Mass.


Arch Neurol. 2006;63(2):234-241. doi:10.1001/archneur.63.2.234.
Text Size: A A A
Published online

Background  Intracranial arteries in the subarachnoid space may compress the brain parenchyma and cranial nerves. Most arterial compressive lesions have been attributed to dolichoectasia in the vertebral-basilar system, and prior reports have concentrated on the pressure effects of basilar artery ectasia. Much less is known about vertebral artery compression of the medulla.

Objective  To describe a series of patients with vertebral arteries compressing the medulla oblongata.

Design  Prospective case studies.

Setting  Tertiary care center.

Patients  Nine symptomatic patients, 4 men and 5 women, between the ages of 32 and 79 years.

Main Outcome Measures  Clinical phenomena, radiographic findings, treatment, and outcomes.

Results  We found that compression most commonly occurs at the ventrolateral surface. The clinical features can be transient or permanent and are predominantly motor and cerebellar or vestibular, but a poor correlation exists between the clinical findings and the severity or extent of impingement. The vertebral arteries were angulated, tortuous, or dilated but not necessarily dolichoectatic to cause obvious indentation. Seven patients were treated with antiplatelets and anticoagulants or analgesics, whereas 2 underwent microvascular decompression, resulting in temporary or no relief. One surgical patient developed cranial nerve complications. Among the medically treated patients, none had progression of deficits, and those with single episodes had no recurrence of symptoms.

Conclusion  This study is the largest collection, to our knowledge, of patients with medullary vascular compression. Further studies are needed to estimate its frequency, natural course, and preferred management.

Figures in this Article

Cerebral arteries in the subarachnoid space may generate pressure and distortion of the brain parenchyma and stretching of the cranial nerves. Most intracranial arterial compressive lesions have been attributed to dolichoectasia, which refers to dilation, enlargement, and tortuosity of vessels.1 Within the cervicocranial arteries, dilatative arteriopathy preferentially involves the vertebrobasilar system. Past reports have emphasized basilar artery ectasia compressing the pons and cranial nerves exiting the pons, causing trigeminal neuralgia and hemifacial spasm24 and also causing pontine infarcts.3,5 Other reports6,7 have described the general features and clinical symptoms of vertebrobasilar dolichoectasia. Compression of the medulla by dilated and/or tortuous vertebral arteries is less well known. We report herein a series of patients with vertebral arteries compressing the medulla oblongata.

From 1998 to 2004, we prospectively collected information on 9 symptomatic patients evaluated by at least 1 of the authors, including clinical phenomena, radiographic findings, treatment, and outcome. All patients underwent magnetic resonance imaging (MRI) and magnetic resonance angiography. The main inclusion criterion was obvious medullary compression by a vertebral artery, which was ectatic, tortuous, or dilated. Patients were excluded if they had dolichoectasia of the basilar artery or if they had other brain or vascular imaging findings that better explained their symptoms and signs. None of the patients had vascular occlusive lesions above the vertebral arteries in the posterior or anterior circulation.

DEMOGRAPHICS

The clinical characteristics of the 9 patients are summarized in Table 1. There were 4 men and 5 women. Ages ranged from 32 to 79 years. There was a bimodal age distribution at initial symptom presentation. Four patients developed their first symptoms in their 30s, and 5 patients first presented at older than 60 years. There were 8 white individuals and 1 African American individual. None of the patients had large artery occlusive lesions.

Table Graphic Jump LocationTable 1. Clinical Features and Radiologic Findings
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 sustained 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. Compression 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 medulla. Only 1 patient (patient 5; Figure 4) had a right vertebral artery that compressed the right medullary surface. This patient also had increased signal on T2-weighted imaging studies within the right medial medulla, representing either wallerian degeneration or damage from branch artery occlusion or compression (Figure 4C). Of note, 3 patients had MRIs that showed enlarged cisterns (Figures 3, 5, and 6).

Place holder to copy figure label and caption
Figure 1.

A 79-year-old man suddenly developed left leg weakness while walking. He leaned on a family member for support until the weakness resolved 5 minutes after onset. Magnetic resonance imaging showed a left vertebral artery pressing on the anterolateral left surface of the medulla.

Graphic Jump Location
Place holder to copy figure label and caption
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).

Graphic Jump Location
Place holder to copy figure label and caption
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).

Graphic Jump Location
Place holder to copy figure label and caption
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).

Graphic Jump Location
Place holder to copy figure label and caption
Figure 5.

A 63-year-old woman developed sudden onset of left hemiparesis and hemisensory loss. Both symptoms resolved after 2 days. Magnetic resonance imaging showed medullary compression along the left anterolateral surface.

Graphic Jump Location
Place holder to copy figure label and caption
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.

Graphic Jump Location
TREATMENT AND CLINICAL COURSE

Six patients were treated conservatively with analgesics, antiplatelets, and anticoagulants, whereas 2 patients had decompressive surgery (patients 7 and 9 in Table 2). Patient 7 had slight postoperative improvement of her hoarseness but developed cranial nerve complications and occipital neuralgia. Patient 9 had temporary relief of symptoms, but episodes recurred 4 months after surgery. The 3 patients with single transient episodes treated conservatively have not had recurrences to date.

Table Graphic Jump LocationTable 2. Management and Subsequent Clinical Course
REPORT OF CASES

We describe 2 patients to illustrate different clinical features.

Patient 4

A 58-year-old man with hypertension suddenly lost his balance while standing near his desk at work and felt his body suddenly being directed to the right. He sensed that the ground was moving underneath him. The episode lasted approximately 20 seconds and did not recur. His neurologic examination results were normal. An MRI was obtained the following day (Figure 3), which showed an ectatic left vertebral artery severely compressing the anterolateral medulla. The MRI showed no acute infarcts on diffusion-weighted imaging and no hemorrhages on susceptibility 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 difficulty 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 abnormalities 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 hamstrings and anterior tibialis with brisk reflexes and a left extensor plantar response. An MRI showed a tortuous right vertebral artery compressing the anterolateral medulla, particularly 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 only slight weakness of the leg extensors.

Medullary compression by the vertebral artery is a little-known clinical entity in the medical literature. There are 14 prior case reports, totaling 19 patients821 (Table 3). We now describe the largest series, to our knowledge, of patients with this condition. From this collection, the major findings were as follows: patients can present with transient symptoms or permanent deficits, motor and vestibular or cerebellar features are the most common clinical presentations, there is a poor correlation between radiographic features and symptoms, and surgery may provide only temporary symptom relief and cause other complications.

Table Graphic Jump LocationTable 3. Prior Reported Cases of Vertebral Artery Compression of the Medulla
CLINICAL AND RADIOLOGIC FEATURES

In our series, the clinical symptoms were variable but mostly consisted of motor and cerebellar or vestibular symptoms and signs. Compression typically occurred along the anterolateral surface, consistent with prior reports (Table 3). The lateral segments of the medulla contain the corticospinal tracts, which when damaged can cause either contralateral or ipsilateral findings depending on the rostral-caudal location of the compression. Two of our patients with hemiparesis had ipsilateral findings, and 1 patient had contralateral findings. In the lateral corticospinal tract, the fibers innervating the lower extremities are located laterally. In patients with transient leg weakness, the clinical features correspond to the topographic distribution of these fibers (Figure 1). Neighboring tracts, such as the spinothalamic and spinocerebellar pathways, did not appear to be involved in our patients, but hypoalgesia and hypothermesthesia were reported in 1 patient with vertebral artery lateral medullary compression.20 Anterolateral compression of the lower cranial nerves or the nucleus ambiguus could explain the vocal cord paralysis in patient 7 and dysphagia and dysphonia seen in previously described patients.14,21 Aural symptoms may be explained by impingement on the cochlear nuclei or the eighth cranial nerve exiting the medulla. Bulbar compression has also been suggested as a possible cause of refractory hypertension22,23 and sleep-disordered breathing,10 but we did not see these features in any of our patients.

In some of our patients, the clinical features did not match the radiographic findings. In particular, patients with transient symptoms such as ataxia or limb weakness had severe medullary compression (Figure 3 and Figure 5) and yet no significant deficits. Patients who had nausea and vertigo did not show compression of the dorsolateral medulla or periventricular nuclei such as the area postrema. However, the possibility exists that ventrolateral impingement could lead to distortion of the dorsolateral areas. Seven of 9 patients had MRIs that showed pyramidal tract involvement 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.

VESSEL DISEASE

The intracranial posterior circulation arteries often show regions of dolichoectasia, which can stretch cranial nerves, compress the brainstem, and cause brain infarcts.6 However, in our series, we found that the vertebral arteries were sometimes tortuous, angulated, and/or dominant but not necessarily elongated and dilated (Figure 2B). Dolichoectasia is therefore not required for the vertebral artery to impinge on the medulla. Several factors likely contribute to the anatomical variations. We found that most of our elderly patients had hypertension and diabetes, which may cause progressive vascular wall damage. Younger patients may have genetic predispositions. For example, dolichoectasia occurs in young patients with Marfan syndrome, acquired immunodeficiency syndrome, sickle cell disease, and Fabry disease.24,25 The young patients in our study (patients 3, 6, 7, and 9) had negative evaluation results for these conditions.

MECHANISMS OF BRAIN INJURY

Vertebral arteriopathies cause neurologic symptoms through multiple mechanisms. Direct medullary compression is the likely cause for certain patients with gradual and persistent symptoms. External compression of brain structures often causes symptoms away from the local region of compression. This may explain why in some patients, the clinical symptoms did not match the location of medullary compression, similar to an expanding extraparenchymatous mass lesion such as a subdural hematoma or congenital anomaly such as Arnold-Chiari malformation. Compression may be gradual, allowing for adaptation, which may reduce the risk of damaging respiratory and autonomic centers in the medulla.

Another potential mechanism is ischemic injury. Compression could generate pressure on perforating branches from the vertebral artery. Traction on these arteries could disrupt blood flow and cause small-vessel infarcts or migrainelike headaches, as seen in patient 3. Elongation and angulation of the intracranial arteries can stretch and distort the orifices of arterial branches. Dilatative arteriopathy, for example, can lead to decreased blood flow in penetrating branches of the basilar artery and cause pontine infarcts.5,26 Transcranial Doppler studies of patients with dolichoectasia have shown abnormal flow patterns. Blood flow is often to and fro within the dilated artery, causing reduced antegrade flow in the vertebrobasilar system.6,27 Blood flow insufficiency under these circumstances can lead to transient ischemic attacks and therefore may be the cause of the transient symptoms seen in some of our patients. Reduced flow can also lead to thrombus formation within the dilated segments, obstruction of penetrating branches by the thrombus, or embolization of clot fragments into the small-vessel perforators.28 Alternatively, atherosclerotic plaques may form along the dilated vessel wall and obstruct the arterial branches.

Patient 5 had an angulated right vertebral artery (Figure 4B) pressing on the lateral surface of the medulla (Figure 4A), and MRI showed a T2 hyperintensity in the medial medulla (Figure 4C). Although the lesion could represent an infarct, a 3-week history of progressive symptoms is atypical for the development of a stroke. The lesion could represent either an unusual “slow stroke” mediated by altered flow in a branch of the vertebral artery or wallerian degeneration.

TREATMENT AND OUTCOME

The best treatment of patients with bulbar compression by a vertebral artery is unknown. In all prior reports except for 3, the patients were treated surgically (Table 3). Almost all of these surgical cases reported significant improvement of deficits after microvascular decompression, although the preoperative and postoperative neurologic examination results and extent of improvement were not reported in detail. The 2 patients we referred for surgery had only slight or temporary improvement and developed complications from new cranial nerve lesions. The 7 other patients were treated conservatively with antiplatelets, anticoagulants, or analgesics, and none had progressive or new symptoms. On the basis of our series of patients, we are reluctant to recommend surgery.

STUDY LIMITATIONS

One of the main limitations of this report is that we cannot be certain that the symptoms in each patient were caused by the radiographic findings; 3 patients (3, 6, and 9) had symptoms that could have been part of a migraine disorder. It would be helpful to compare our symptomatic group with an asymptomatic population with vertebral artery compression of the medulla. We have encountered patients with apparently asymptomatic compression but have not systematically studied this phenomenon, and there is no literature on asymptomatic compression. We now are embarking on a prospective blind study looking at MRIs to attempt to answer this query.

In conclusion, medullary compression from a vertebral artery can cause a wide spectrum of clinical presentations, from sudden transient events to persistent deficits and from lower cranial nerve findings to respiratory and autonomic changes. Contrary to prior reports, microvascular decompression does not always relieve symptoms. Future studies are needed to estimate the true frequency of medullary vascular compression, its natural history, and its preferred treatment.

Correspondence: Sean I. Savitz, MD, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215 (ssavitz@bidmc.harvard.edu).

Accepted for Publication: September 27, 2005.

Author Contributions:Study concept and design: Savitz, Ronthal, and Caplan. Acquisition of data: Savitz and Caplan. Analysis and interpretation of data: Savitz and Caplan. Drafting of the manuscript: Savitz and Caplan. Critical revision of the manuscript for important intellectual content: Savitz, Ronthal, and Caplan. Administrative, technical, and material support: Savitz and Ronthal. Study supervision: Ronthal and Caplan.

Funding/Support: This work was supported in part by the Fellow to Faculty Transition Award (Dr Savitz) from the American Heart Association, Dallas, Tex.

Caplan  LR Dilatative arteriopathy (dolichoectasia): what is known and not known. Ann Neurol 2005;57469- 471
PubMed Link to Article
Boeri  RPasserini  A The megadolichobasilar anomaly. J Neurol Sci 1964;11475- 484
PubMed Link to Article
Nishizaki  TTamaki  NTakeda  NShirakuni  TKondoh  TMatsumoto  S Dolichoectatic basilar artery: a review of 23 cases. Stroke 1986;171277- 1281
PubMed Link to Article
Garibaldi  DCMiller  NR Tortuous basilar artery as cause of hemifacial spasm. Arch Neurol 2003;60626- 627
PubMed Link to Article
Pessin  MSChimowitz  MILevine  SR  et al.  Stroke in patients with fusiform vertebrobasilar aneurysms. Neurology 1989;3916- 21
PubMed Link to Article
Schwartz  ARWHennerici  M Dolichoectatic intracranial arteries: review of selected aspects. Cerebrovasc Dis 1993;3273- 279
Link to Article
Baquero  MYaya-Huaman  R Vertebrobasilar dolichoectasia [in Spanish]. Rev Neurol 1998;26143- 148
PubMed
Kim  PIshijima  BTakahashi  HShimizu  HYokochi  M Hemiparesis caused by vertebral artery compression of the medulla oblongata: case report. J Neurosurg 1985;62425- 429
PubMed Link to Article
Maruyama  KTanaka  MIkeda  STada  TYanagisawa  N A case report of quadriparesis due to compression of the medulla oblongata by the elongated left vertebral artery [in Japanese]. Rinsho Shinkeigaku 1989;29108- 111
PubMed
Miyazaki  MHashimoto  TSakurama  NYoshimoto  TTayama  MKuroda  Y Central sleep apnea and arterial compression of the medulla. Ann Neurol 1991;29564- 565
PubMed Link to Article
Vincentelli  FCaruso  GRabehanta  PBRey  M Surgical treatment of a rare congenital anomaly of the vertebral artery: case report and review of the literature. Neurosurgery 1991;28416- 420
PubMed Link to Article
Hongo  KKobayashi  SHokama  MSugita  K Vertebral artery section for treating arterial compression of the medulla oblongata: case report. J Neurosurg 1993;79116- 118
PubMed Link to Article
Moss  MSWest  RJ Ectasia of the vertebral artery as a cause of isolated pyramidal tract signs: case report and a review of the literature. Br J Neurosurg 1996;10497- 499
PubMed Link to Article
Hongo  KNakagawa  HMorota  NIsobe  M Vascular compression of the medulla oblongata by the vertebral artery: report of two cases. Neurosurgery 1999;45907- 910
PubMed Link to Article
Salvi  FMascalchi  MBortolotti  C  et al.  Hypertension, hyperekplexia, and pyramidal paresis due to vascular compression of the medulla. Neurology 2000;551381- 1384
PubMed Link to Article
Meyer  MADavid  CEChahin  NS Palatal myoclonus secondary to vertebral artery compression of the inferior olive. J Neuroimaging 2000;10221- 223
PubMed
Koyama  SMaeda  TKomine  A Medulla and upper cervical cord compression by bilateral vertebral artery presented with myelopathy and drop attack: case report [in Japanese]. No To Shinkei 2002;54435- 439
PubMed
Takano  SSaitoh  MMiyasaka  YFujii  KTakagi  H A case report of hemiparesis due to compression of the medulla oblongata by an elongated vertebral artery [in Japanese]. No Shinkei Geka 2001;29247- 251
PubMed
Ubogu  EEChase  CMVerrees  MAMetzger  AKZaidat  OO Cervicomedullary junction compression caused by vertebral artery dolichoectasia and requiring surgical treatment: case report. J Neurosurg 2002;96140- 143
PubMed Link to Article
Iwasaki  YNakamura  THamada  K Hypoalgesia and hypothermesthesia in a lower extremity due to compression of the medulla oblongata by an elongated vertebral artery [in Japanese]. Rinsho Shinkeigaku 2004;44176- 181
PubMed
Tomasello  FAlafaci  CSalpietro  FMLongo  M Bulbar compression by an ectatic vertebral artery: a novel neurovascular construct relieved by microsurgical decompression. Neurosurgery 2005;56117- 124
PubMed Link to Article
Levy  EIClyde  BMcLaughlin  MRJannetta  PJ Microvascular decompression of the left lateral medulla oblongata for severe refractory neurogenic hypertension. Neurosurgery 1998;431- 9
PubMed Link to Article
Ishikawa  TNagayama  MIida  MShinohara  Y Bulbovascular compression by megadolichobasilar artery manifested as neurogenic and refractory hypertension [in Japanese]. Rinsho Shinkeigaku 2004;44359- 364
PubMed
Zambrino  CABerardinelli  AMartelli  AVercelli  PTermine  CLanzi  G Dolicho-vertebrobasilar abnormality and migraine-like attacks. Eur Neurol 1999;4110- 14
PubMed Link to Article
Mitsias  PLevine  SR Cerebrovascular complications of Fabry's disease. Ann Neurol 1996;408- 17
PubMed Link to Article
Passero  SFilosomi  G Posterior circulation infarcts in patients with vertebrobasilar dolichoectasia. Stroke 1998;29653- 659
PubMed Link to Article
Hennerici  MRautenberg  WSchwartz  A Transcranial Doppler ultrasound for the assessment of intracranial arterial flow velocity–part 2: evaluation of intracranial arterial disease. Surg Neurol 1987;27523- 532
PubMed Link to Article
De Georgia  MBelden  JPao  LPessin  MKwan  ECaplan  L Thrombus in vertebrobasilar dolichoectatic artery treated with intravenous urokinase. Cerebrovasc Dis 1999;928- 33
PubMed Link to Article

Figures

Place holder to copy figure label and caption
Figure 1.

A 79-year-old man suddenly developed left leg weakness while walking. He leaned on a family member for support until the weakness resolved 5 minutes after onset. Magnetic resonance imaging showed a left vertebral artery pressing on the anterolateral left surface of the medulla.

Graphic Jump Location
Place holder to copy figure label and caption
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).

Graphic Jump Location
Place holder to copy figure label and caption
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).

Graphic Jump Location
Place holder to copy figure label and caption
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).

Graphic Jump Location
Place holder to copy figure label and caption
Figure 5.

A 63-year-old woman developed sudden onset of left hemiparesis and hemisensory loss. Both symptoms resolved after 2 days. Magnetic resonance imaging showed medullary compression along the left anterolateral surface.

Graphic Jump Location
Place holder to copy figure label and caption
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.

Graphic Jump Location

Tables

Table Graphic Jump LocationTable 1. Clinical Features and Radiologic Findings
Table Graphic Jump LocationTable 2. Management and Subsequent Clinical Course
Table Graphic Jump LocationTable 3. Prior Reported Cases of Vertebral Artery Compression of the Medulla

References

Caplan  LR Dilatative arteriopathy (dolichoectasia): what is known and not known. Ann Neurol 2005;57469- 471
PubMed Link to Article
Boeri  RPasserini  A The megadolichobasilar anomaly. J Neurol Sci 1964;11475- 484
PubMed Link to Article
Nishizaki  TTamaki  NTakeda  NShirakuni  TKondoh  TMatsumoto  S Dolichoectatic basilar artery: a review of 23 cases. Stroke 1986;171277- 1281
PubMed Link to Article
Garibaldi  DCMiller  NR Tortuous basilar artery as cause of hemifacial spasm. Arch Neurol 2003;60626- 627
PubMed Link to Article
Pessin  MSChimowitz  MILevine  SR  et al.  Stroke in patients with fusiform vertebrobasilar aneurysms. Neurology 1989;3916- 21
PubMed Link to Article
Schwartz  ARWHennerici  M Dolichoectatic intracranial arteries: review of selected aspects. Cerebrovasc Dis 1993;3273- 279
Link to Article
Baquero  MYaya-Huaman  R Vertebrobasilar dolichoectasia [in Spanish]. Rev Neurol 1998;26143- 148
PubMed
Kim  PIshijima  BTakahashi  HShimizu  HYokochi  M Hemiparesis caused by vertebral artery compression of the medulla oblongata: case report. J Neurosurg 1985;62425- 429
PubMed Link to Article
Maruyama  KTanaka  MIkeda  STada  TYanagisawa  N A case report of quadriparesis due to compression of the medulla oblongata by the elongated left vertebral artery [in Japanese]. Rinsho Shinkeigaku 1989;29108- 111
PubMed
Miyazaki  MHashimoto  TSakurama  NYoshimoto  TTayama  MKuroda  Y Central sleep apnea and arterial compression of the medulla. Ann Neurol 1991;29564- 565
PubMed Link to Article
Vincentelli  FCaruso  GRabehanta  PBRey  M Surgical treatment of a rare congenital anomaly of the vertebral artery: case report and review of the literature. Neurosurgery 1991;28416- 420
PubMed Link to Article
Hongo  KKobayashi  SHokama  MSugita  K Vertebral artery section for treating arterial compression of the medulla oblongata: case report. J Neurosurg 1993;79116- 118
PubMed Link to Article
Moss  MSWest  RJ Ectasia of the vertebral artery as a cause of isolated pyramidal tract signs: case report and a review of the literature. Br J Neurosurg 1996;10497- 499
PubMed Link to Article
Hongo  KNakagawa  HMorota  NIsobe  M Vascular compression of the medulla oblongata by the vertebral artery: report of two cases. Neurosurgery 1999;45907- 910
PubMed Link to Article
Salvi  FMascalchi  MBortolotti  C  et al.  Hypertension, hyperekplexia, and pyramidal paresis due to vascular compression of the medulla. Neurology 2000;551381- 1384
PubMed Link to Article
Meyer  MADavid  CEChahin  NS Palatal myoclonus secondary to vertebral artery compression of the inferior olive. J Neuroimaging 2000;10221- 223
PubMed
Koyama  SMaeda  TKomine  A Medulla and upper cervical cord compression by bilateral vertebral artery presented with myelopathy and drop attack: case report [in Japanese]. No To Shinkei 2002;54435- 439
PubMed
Takano  SSaitoh  MMiyasaka  YFujii  KTakagi  H A case report of hemiparesis due to compression of the medulla oblongata by an elongated vertebral artery [in Japanese]. No Shinkei Geka 2001;29247- 251
PubMed
Ubogu  EEChase  CMVerrees  MAMetzger  AKZaidat  OO Cervicomedullary junction compression caused by vertebral artery dolichoectasia and requiring surgical treatment: case report. J Neurosurg 2002;96140- 143
PubMed Link to Article
Iwasaki  YNakamura  THamada  K Hypoalgesia and hypothermesthesia in a lower extremity due to compression of the medulla oblongata by an elongated vertebral artery [in Japanese]. Rinsho Shinkeigaku 2004;44176- 181
PubMed
Tomasello  FAlafaci  CSalpietro  FMLongo  M Bulbar compression by an ectatic vertebral artery: a novel neurovascular construct relieved by microsurgical decompression. Neurosurgery 2005;56117- 124
PubMed Link to Article
Levy  EIClyde  BMcLaughlin  MRJannetta  PJ Microvascular decompression of the left lateral medulla oblongata for severe refractory neurogenic hypertension. Neurosurgery 1998;431- 9
PubMed Link to Article
Ishikawa  TNagayama  MIida  MShinohara  Y Bulbovascular compression by megadolichobasilar artery manifested as neurogenic and refractory hypertension [in Japanese]. Rinsho Shinkeigaku 2004;44359- 364
PubMed
Zambrino  CABerardinelli  AMartelli  AVercelli  PTermine  CLanzi  G Dolicho-vertebrobasilar abnormality and migraine-like attacks. Eur Neurol 1999;4110- 14
PubMed Link to Article
Mitsias  PLevine  SR Cerebrovascular complications of Fabry's disease. Ann Neurol 1996;408- 17
PubMed Link to Article
Passero  SFilosomi  G Posterior circulation infarcts in patients with vertebrobasilar dolichoectasia. Stroke 1998;29653- 659
PubMed Link to Article
Hennerici  MRautenberg  WSchwartz  A Transcranial Doppler ultrasound for the assessment of intracranial arterial flow velocity–part 2: evaluation of intracranial arterial disease. Surg Neurol 1987;27523- 532
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