Left Posterior Inferior Cerebellar Artery Research Articles

Vertebral Artery Compression during Roll Tilt: Is the Edge of the Foramen Magnum a Culprit?

Dear Editor, Rotatory vertebral artery occlusion (RVAO) indicates a mechanical compression of the vertebral artery (VA) in certain head positions.1 In typical RVAO, the arterial occlusion occurs mostly at the high cervical level (atlantoaxis) during contralateral head turning.2 There is a single report of RVAO during head tilt;3 however, the exact structure responsible for compressing the VA in that case was not established. We report here another case of tilt-induced RVAO and discuss the role of the foramen magnum in its etiology. A 64-year-old man presented with positional vertigo of 1 month duration. The patient specifically indicated that the vertigo occurred without tinnitus and within 5-10 seconds of tilting his head to the left. Positional maneuvers including supine head roll and the Dix-Hallpike maneuver on both sides evoked neither vertigo nor nystagmus. However, a leftward head tilt while upright induced right-beating nystagmus, which changed to left-beating nystagmus after 25 seconds. There was no obvious vertical or torsional component (Fig. 1A). A rightward head tilt evoked neither vertigo nor nystagmus. MRI revealed no parenchymal lesion in the brainstem or cerebellum. However, CT angiography demonstrated occlusion of the right VA, and a severe stenosis at the intracranial segment of the VA just above the origin of the posterior inferior cerebellar artery (PICA). In addition, the stenotic segment of the left VA was spatially close to the edge of the foramen magnum, which probably compressed the stenotic segment of the left VA during ipsilesional head tilting (Fig. 1B). Proximal left VA duplex ultrasonography revealed blunting of the dynamic arterial flow and decreased peak systolic flow velocity during leftward head tilt (Fig. 1C). The right VA and PICA were visualized by a retrograde flow from the left VA on digital subtraction angiography. After balloon angioplasty and intravascular stenting of the stenotic left VA segment, the patient's symptoms completely resolved, and he did not experience recurrence during the immediate 1-year follow-up. Fig. 1 Findings of rotational vertebral-artery occlusion during roll tilt. A: Electronystagmography. Leftward head tilt evokes an initial right-beating nystagmus for 10 s, followed by 15 s of a null period and then left-beating nystagmus. There is no obvious ... While confirmatory dynamic angiography was not performed, the anatomical relationship, the duplex ultrasonographic findings, and the outcome of intervention on the stenotic VA segment led to a diagnosis of RVAO during head tilt. Of particular interest was that the symptoms of RVAO disappeared after intra-arterial intervention in our patient, even though the procedure did not remove the speculated medial edge of the foramen magnum. However, given that normal subjects did not experience vertigo during head tilt and the RVAO was resolved after intra-arterial intervention in the present case, the underlying focal stenosis of the dominant VA must have contributed to the development of RVAO during head tilt. Down-beat nystagmus with mixed horizontal and torsional components have been found in patients with RVAO in several studies, and it has been suggested that transient ischemia-induced superior labyrinth excitation is the mechanism underlying the nystagmus.1 In the present case, the left PICA branched out before the stenotic VA segment; therefore, the initial right-beating nystagmus and subsequent left-beating nystagmus in this patient can be ascribed to transient ischemia-induced asymmetrical excitation and inhibition of the right labyrinthine. Alternatively, the initial right-beating nystagmus might have been generated by ischemia of the right cerebellum. The left medial vestibular nucleus, which is supplied directly by the left VA perforators, is also a candidate for generation of the initial nystagmus. The absence of tinnitus and the vertical and torsional components of the nystagmus might favor the latter mechanism. The evolution into left-beating nystagmus could be attributed to a compensatory mechanism.1,2 However, the lack of evidence regarding the perfusion status leaves the exact mechanism of nystagmus uncertain. In conclusion, arterial compression at the edge of the foramen magnum should be suspected when RVAO occurs during head tilting. Intra-arterial intervention may be considered as a treatment option.

Cervical osteophyte causing cerebellar infarction

A 59-year-old man presented with sudden onset of vertigo, headache, nausea, and left-hand clumsiness. Neurological examination showed multidirectional nystagmus and left kinetic cerebellar syndrome. The patient did not have neck injury. Brain MRI showed acute infarction in the region of the left posterior inferior cerebellar artery (fi gure A). CT angiography showed left vertebral artery stenosis caused by extrinsic compression by an osteophyte of the superior articular process of the fourth cervical vertebra, compromising the foramen transversarium, with a downstream occlusion of the left vertebral artery in its extracranial segment (fi gure B, C). Extrinsic compression of the vertebral artery is a rare complication of cervical osteophytes. Embolic infarction rarely occurs. Surgical treatment can be proposed to decompress the artery.

Vertebral artery variations in thoracic aortic patients

Arterial variation is common in the vertebral artery, and simple occlusion of the left subclavian artery may result in brain infarction, especially when it terminates in the posterior inferior cerebellar artery (PICA). We report the results of preoperative vertebral artery evaluation by magnetic resonance angiography (MRA) and its impact upon operative strategy. Among the 214 patients who underwent thoracic aortic surgery from 2009 through 2012, 159 patients with preoperative MRA were retrospectively analysed. Patients' age ranged from 35 to 88 (median 72), 122 were male and 115 had degenerative aneurysms. Prevalence rates of vertebral artery variations and occlusive lesions were reported, together with operative strategies and outcomes. There were 19 hypoplasia (12%), 10 PICA termination (6%) and 12 occlusive lesion (8%) on the right vertebral artery and 10 hypoplasia (6%), 5 PICA termination (3%), 7 direct arch origin (4%) and 3 occlusive lesion (2%) on the left. Two of the seven arch-originated arteries terminated in the PICA. In aortic arch replacement, these were reconstructed together with the left subclavian artery while hypothermia was maintained. During thoracic endovascular aortic repair with Zone-2 proximal landing, debranching bypass was employed to preserve left subclavian perfusion when there was PICA termination, hypoplasia or occlusive lesion. In 1 patient with hypoplasia between the basilar artery and the left PICA, bypass was added immediately after deployment because radial pressure dropped critically. No brain infarction occurred with this strategy. PICA termination and right side hypoplasia/occlusive lesion, where left subclavian perfusion is important for brain protection, is present in ∼ 30%. Left vertebral artery that originated from the arch should be managed with care, because PICA termination is highly prevalent.

Role of high-resolution magnetic resonance imaging in the diagnosis of primary angiitis of the central nervous system.

BackgroundPrimary angiitis of the central nervous system (PACNS) is a rare disorder and is often difficult to diagnose due to the lack of a confirmatory test. PACNS can generally be diagnosed based on typical angiographic findings. We describe herein a patient diagnosed with PACNS despite the presence of normal findings on conventional angiography.Case ReportA 44-year-old man with a recent history of ischemic stroke in the right posterior cerebral artery territory developed acute-onset vertigo. Diffusion-weighted imaging revealed an acute infarction within the left posterior inferior cerebellar artery. His medical history was unremarkable except for hyperlipidemia; the initial examination revealed mild gait imbalance. During the 10 days of hospital admission, the patient experienced four recurrent ischemic strokes within the posterior circulation territory (occipital lobe, pons, and cerebellum). He was diagnosed with recurrent cerebral infarctions due to PACNS. The basilar artery exhibited no demonstrable luminal stenosis, but there were direct imaging signs of central nervous system angiitis including wall thickening and contrast enhancement. High-dose intravenous steroid therapy followed by oral prednisolone was administered. There was no further stroke recurrence and follow-up imaging of the arterial walls showed normalization of their characteristics.ConclusionsThe present case emphasizes the importance of wall imaging in the diagnosis and treatment of PACNS.

発達した後下小脳動脈に発生した解離性動脈瘤

We report a rare case of dissecting aneurysm of the posterior inferior cerebellar artery (PICA) with vascular variation. A 38-year-old man, who had no medical, familial or traumatic histories, presented with headache, nausea and mild consciousness disturbance. Computed tomography (CT) imaging demonstrated subarachnoid hemorrhage with intra-ventricular hemorrhage. Angiography disclosed an aneurysm of left PICA, which did not involve the vertebral artery. The PICA was well developed and widely perfused the cerebellum and lower brain stem, which was accompanied by lack of ipsi-lateral anterior inferior cerebellar artery (AICA) and contra-lateral PICA. The aneurysm was successfully treated by trapping and revascularization procedure with occipital artery (OA)-PICA anastomosis. We suggest that congenital vascular variation related to well-developed PICA might lead to dissecting aneurysm, and that direct surgical treatment with bypass would be indicated for such patients to preserve hemodynamic integrity.

Spontaneous Heparin-Induced Thrombocytopenia Syndrome: Two New Cases and a Proposal For Defining This Disorder

IntroductionHeparin-induced thrombocytopenia (HIT) is a transient, autoimmune-like, prothrombotic disorder caused by heparin-dependent, platelet-activating IgG reactive against platelet factor 4/heparin (PF4/H). There is an emerging literature (Am J Med 2008;121:632-6. J Thromb Haemost 2008;6:1598-1600; Thromb Haemost 2013;109:669-75) pointing to rare instances of “spontaneous” HIT in patients without preceding heparin. We report 2 new cases and propose a definition for this controversial disorder. CASE #1. A 62-y.o. man presented with left middle cerebral artery stroke and thrombocytopenia (platelet count, 65×109/L). There was no previous history of thrombocytopenia, surgery, hospitalization, or heparin exposure. Clot extraction performed with heparin was complicated by further platelet count decline to 27 (nadir) and progressive thrombosis of the carotid artery. Aspirin was started, and the platelets recovered to >150 by day 13. CASE #2. A 54-y.o. female developed right leg swelling, left-upper extremity weakness/paresthesias, and thrombocytopenia (61×109/L) 15 days post-shoulder hemiarthroplasty; no intra-/postoperative heparin had been given. Brain MRI demonstrated acute infarct in the left posterior inferior cerebellar artery territory; angiography showed non-visualization of the left vertebral artery. Ultrasound revealed right lower-limb deep-vein thrombosis. Heparin treatment resulted in further platelet count fall to 37 (nadir). Treatment with argatroban, followed by fondaparinux, was associated with platelet count recovery to >150 by day 39. MethodsTesting for HIT antibodies was performed by commercial EIA-IgG/A/M (Immucor GTI Diagnostics), in-house EIA-IgG (McMaster), and serotonin-release assay (SRA). ResultsBoth patients' sera (obtained before any heparin administration) tested strongly positive for HIT antibodies (Table), including strong platelet activation at 0.1 and 0.3 IU/mL heparin, as well as at 0 U/mL heparin, with no platelet activation at 100 IU/mL heparin: these serological features are characteristic of “delayed-onset HIT” (Ann Intern Med 2001;135:502-6). Antibody reactivity declined markedly by 2 to 4 weeks (including loss of platelet-activating properties at 0 IU/mL heparin), in keeping with the usual transience of HIT antibodies (N Engl J Med 2001;344:1286-92), and paralleling both patients' platelet count recovery. DiscussionThese cases further support spontaneous HIT as an unusual explanation for acute arterial stroke and thrombocytopenia. One patient had preceding orthopedic surgery, an event previously reported with spontaneous HIT (Thromb Haemost 2013;109:669-75). The strong serum-dependent platelet activation at 0 IU/mL heparin helps to explain how thrombocytopenia and thrombosis can occur in a patient not receiving heparin. RECOMMENDATION. Based on the serological findings of these and previous cases, we propose that a definitive diagnosis of spontaneous HIT syndrome should be based upon all of the following criteria: thrombocytopenia, thrombosis, lack of proximate heparin exposure, strong-positive PF4-dependent immunoassay(s), and a strong-positive platelet activation assay featuring both heparin-dependent (e.g., high heparin neutralization) and heparin-independent platelet activation (at 0 IU/mL heparin). Disclosures:Warkentin:Pfizer Canada: Honoraria; Paringenix: Consultancy; Immucor GTI Diagnostics: Research Funding; WL Gore: Consultancy; GSK: Research Funding.

Cervical spondylosis: a rare and curable cause of vertebrobasilar insufficiency

Spondylotic vertebral artery (VA) compression is a rare cause of vertebrobasilar insufficiency and stroke. A 53-year-old man experienced multiple brief vertebrobasilar transient ischemic attacks (TIAs) and strokes, not apparently triggered by neck movements. Brain magnetic resonance imaging (MRI) documented consecutive infarcts, first in the left then right medial posterior inferior cerebellar artery (PICA) territories. Angiography showed two extracranial right vertebral artery (VA) stenoses, left VA hypoplasia, absence of left PICA and a dominant right PICA. Computed tomography angiography revealed right VA compression by osteophytes at C5-C6 and C6-C7 levels. No further vertebrobasilar insufficiency symptoms occurred in the 65 months following VA surgical decompression. Our literature review found 49 published surgical cases with vertebrobasilar symptoms caused by cervical spondylosis. Forty cases had one or more brief TIAs frequently triggered by neck movements. Three cases presented with stroke without prior TIA, with symptoms suggesting a top of the basilar artery embolic infarcts (one combined with a PICA infarct). Six cases had both TIAs and minor stroke. VA compression by uncovertebral osteophytes at the C5-C6 level was common. Dynamic angiography done in 38 cases systematically revealed worsening of VA stenosis or complete occlusion with either neck extension or rotation (ipsilateral when specified). Contralateral VA incompetence was found in 14 patients. Spondylotic VA stenosis can cause hemodynamic TIAs and watershed strokes, especially when contralateral VA insufficiency is combined to specific neck movements. Low-amplitude neck movement may suffice in severe cases. Embolic vertebrobasilar events are less frequent. VA decompression from spondylosis may prevent recurrent ischemic episodes.

Fenestrated vertebral artery

Fenestrations of the vertebral arteries (VAs) are usually identified angiographically. A left fenestrated vertebral artery (fVA) is reported here, identified in an adult specimen by microdissection. The distal segment of this VA was fenestrated and it consisted of two arms, the caudal one being larger than the cranial one. The caudal end of the rostral arm and the left posterior inferior cerebellar artery (PICA) were inserted at the same point. The anterior spinal artery was leaving the caudal arm of the fVA. On that side the anterior inferior cerebellar artery (AICA) was rudimentary, its cerebellar hemispheric territory being supplied by the PICA. The rostral arm of the fVA and the AICA were united by an anastomosis coursing on the ventral side of the olive. The AICA-to-fVA anastomosis, as well as the PICA, were supplying perforator arteries of the retro-olivary sulcus. Anatomical details of various arterial morphologies are important during specific surgical and interventional procedures.

A Juvenile Case of Cerebellar Arteriovenous Malformation with Gradual Onset of Dysphoria and Headache

A 25-year-old woman was admitted because of frequent vomiting and headache which had lasted over one week. She had initially clear consciousness but slowly progressive mild headache and dysphoria. Emergency cranial CT revealed a 4 cm haematoma in the left cerebellar hemisphere. CT angiography showed a 2×2 cm nidus of an arteriovenous malformation (AVM) in the left hemisphere fed from the left posterior inferior cerebellar artery and draining into the inferior hemispheric vein. We performed a surgical resection of the AVM after decompression therapy to counteract the brain oedema. She recovered completely without any neurological deficits. This case recalls the importance of cooperation between diagnostic neuroradiology and neurosurgery in emergency, considering AVM, even if infrequent, among possible diseases.

Coil Embolization of Intracranial Aneurysm in Polyarteritis Nodosa

Polyarteritis nodosa (PAN) is a rare multisystem disease characterized by systemic necrotizing arteritis of small and medium size arteries. The skin, joints, kidneys, gastrointestinal tract and peripheral nerves are most commonly involved. Although aneurysms are commonly seen in the visceral vessels, intracranial aneurysms are rare with 15 reported cases. The intracranial aneurysms are usually multiple and located in supra- as well as infra-tentorial compartments. Most of the cases presented with subarachnoid or parenchymal hemorrhage. The aneurysms were usually small, although large cavernous aneurysms were reported in one case. Treatment guidelines are not clear regarding the management of these cases. Most patients were treated conservatively by medical management with surgical excision performed in only two cases and coiling done in one patient with cavernous aneurysms. Repeat hemorrhages or re-bleed in spite of medical treatment have also been reported. We describe the case of a 22-year-old woman, a known case of PAN who presented with subarachnoid hemorrhage. Cerebral angiogram showed a ruptured right middle cerebral artery bifurcation aneurysm along with unruptured left middle cerebral, right posterior communicating and left posterior inferior cerebellar artery aneurysms. Her previous abdominal angiogram had revealed multiple aneurysms in visceral arteries. Successful coil embolization of the ruptured right MCA bifurcation aneurysm was performed with preservation of the parent vessel. The patient made a complete recovery and was placed on medical treatment for PAN. Follow-up MR angiography at three months revealed stable occlusion of the embolized aneurysm with no change in the unruptured aneurysms. Although rare, PAN can be associated with intracranial aneurysms which can cause subarachnoid or parenchymal hemorrhage. Selected cases can be treated safely by coil embolization.

Intractable Occipital Neuralgia Caused by an Entrapment in the Semispinalis Capitis

Occipital neuralgia is a rare pain syndrome characterized by periodic lancinating pain involving the occipital nerve complex. We present a unique case of entrapment of the greater occipital nerve (GON) within the semispinalis capitis, which was thought to be the cause of occipital neuralgia. A 66-year-old woman with refractory left occipital neuralgia revealed an abnormally low-loop of the left posterior inferior cerebellar artery on the magnetic resonance imaging, suggesting possible vascular compression of the upper cervical roots. During exploration, however, the GON was found to be entrapped at the perforation site of the semispinalis capitis. There was no other compression of the GON or of C1 and C2 dorsal roots in their intracranial course. Postoperatively, the patient experienced almost complete relief of typical neuralgic pain. Although occipital neuralgia has been reported to occur by stretching of the GON by inferior oblique muscle or C1-C2 arthrosis, peripheral compression in the transmuscular course of the GON in the semispinalis capitis as a cause of refractory occipital neuralgia has not been reported and this should be considered when assessing surgical options for refractory occipital neuralgia.

English

Introduction Anomalies and variations of the anterior communicating artery are common. Fenestration has been reported as the most common variation of this artery. Dolichoectasia of intracranial arteries is a rare arteriopathy characterised by elongation and widening of the arteries, mostly involving vertebral and basilar arteries. This report discusses large anterior communicating artery fenestration associated with posterior circulation anomalies. Case Report We report here a rare case of large anterior communicating artery fenestration associated with mild dolichoectasia of the basilar artery and marked dolichoectasia of the left posterior inferior cerebellar artery, forming a large vascular loop at the area of cisterna magna, as well as hypoplasia of the left anterior inferior cerebellar artery. The study discusses the details of this case. Conclusion Dolichoectasia of intracranial arteries is a rare arteriopathy characterised by elongation and widening of the arteries and disturbance of the laminar blood flow, mostly involving vertebral and basilar arteries.

Profound Gastroparesis after Bilateral Posterior Inferior Cerebellar Artery Territory Infarcts (P01.030)

Objective: To describe a case of acute gastroparesis as a result of medullary infarction. Background Function of the gastrointestinal system is partially dependent upon the integrity of the lower brain stem. While dysphagia commonly results from strokes of varying locations, acute dysfunction of other segments of the alimentary canal from stroke is not a well-described phenomenon. Design/Methods: Case report. Results: A 65 year old man with a history of diabetes mellitus without previous gastrointestinal difficulty presented with sudden onset vertigo, nausea, vomiting, a left Horner9s syndrome and hemiataxia, as well as gait ataxia. Magnetic resonance imaging (MRI) revealed an acute infarction in the midline cerebellum bilaterally and the left posterior caudal medulla, all within the right and left posterior inferior cerebellar artery (PICA) territories. Over the following week, the persistent nausea, vomiting, and vertigo gave way to severe nausea and vomiting exclusively after eating, accompanied by instantaneous satiety. Brain imaging demonstrated acute infarction of the midline cerebellum bilaterally and the left posterior caudal medulla. Serial cranial CT scans revealed minimal changes; a contrast-enhanced abdominal CT and endoscopy showed severe gastric distention but no anatomical obstruction of the gut. A gastric emptying study demonstrated 99% retention of the radiolabled meal on serial scintigraphy after 2, 3, and 4 hours post-ingestion, with minimal activity seen in the duodenum, consistent with severe gastroparesis. His symptoms were refractory to medical management, and he required a jejunostomy tube for 8 weeks as his oral intake gradually improved. Conclusions: Acute, isolated gastroparesis without gastrointestinal pathology can result from medullary infarctions. A possible explanation may be infarction or edema particularly affecting the pars centralis of the nucleus of the tractus solitarius. Preexisting diabetes mellitus may also have been a predisposing factor. Disclosure: Dr. Liff has received personal compensation for activities with E-Rewards Medical. Dr. Labovitz has nothing to disclose. Dr. Robbins has nothing to disclose.

A Naturalistic On-Off-On Trial of Dextromethorphan/Quinidine for Agitation Associated with Cerebellar Injury

Mr. A, a 47 year-old man with a complicated medical history including HIV and neurovascular syphilis, presented to an urban academic medical center with complaints of headache, vertigo, facial numbness, and intractable hiccups. He reported being awakened from sleep by a loud popping sound coming from the back of his neck with immediate onset of his presenting symptoms. Exam was remarkable for dysarthric speech and copious oral secretions that he was unable to swallow. Magnetic resonance imaging of the brain revealed areas of restricted diffusion in the left inferior cerebellar hemisphere and the left lateral aspect of the medulla consistent with an acute infarct of the left posterior inferior cerebellar artery (PICA). Subsequent CT angiography revealed an occlusion of the left vertebral artery thought to be due to dissection. Psychiatry was consulted on the 13th hospital day due to worsening episodic agitation that had begun on the 7th hospital day. He was noted to have very poor frustration tolerance, often becoming upset with his dietary restrictions and perceived delay in responses to his requests. He had pulled out his intravenous (IV) lines on several occasions and had pushed over his IV pole. Psychiatric consultation had finally been prompted by nursing becoming upset that Mr. A was watching pornography on his laptop

Spinal arachnoiditis and cyst formation with subarachnoid haemorrhage

We present the case of a 58-year-old lady with p-ANCA vasculitis who suffered a WFNS grade 1 subarachnoid haemorrhage (Fisher grade 1) secondary to a ruptured left posterior inferior cerebellar artery aneurysm and then developed a rare complication of radiologically progressive spinal arachnoiditis despite maintained clinical response to definitive treatment measures.

Ruptured Aneurysm of a Posterior Inferior Cerebellar Artery Communicating Artery

A hypertensive 60-year-old man presented with a rare aneurysm arising from the posterior inferior cerebellar artery (PICA) communicating artery, manifesting as subarachnoid hemorrhage with intraventricular hemorrhage. Angiography showed a small aneurysm arising from a fine and tortuous artery interconnecting the bilateral vermian branches of distal PICAs. The right PICA was absent and its vermian territory was supplied by the left PICA through this communicating artery. The right anterior inferior cerebellar artery was also connected to the vermian branch of the right PICA. At surgery, a reddish and apparent fusiform aneurysm was noted at the top of the arterial loop under the cerebellar vermis. Microsurgical trapping and removal of the aneurysm was performed without complication. Histological examination demonstrated typical findings of a true aneurysm. Only four previous cases of aneurysm of the communicating artery between the bilateral distal PICAs have been reported. In all five reported cases including ours, the PICA communicating artery contributed to the collateral blood supply of the contralateral vermian territory based on vascular anomalies. Hemodynamic stress and congenital vulnerability may have caused this aneurysm. Trapping is suitable to treat this precarious aneurysm if other collateral vessels supply the contralateral vermian territory.

Hemifacial Spasm due to Compression of the Posterior Inferior Cerebellar Artery Aneurysm Treated with Botulinum Toxin Type-A: A Case Report

A 79-year-old female presented with five months history of progressive involuntary twitching movement on left face. Brain MR imaging revealed a heterogeneous T2 hyperintense lesion at left cerebellopontine angle. CT angiography showed a partially thrombosed saccular aneurysm of left PICA (posterior inferior cerebellar artery). The patient was treated with Botulinum toxin type A and almost total relief of symptoms was noticed during one month followup. Botulinium toxin injection is an effective symptomatic treatment option in nonsurgical secondary hemifacial spasm (HFS) cases.

Head Injury Football Player

HISTORY: 17 year-old junior high school football defensive end sustained a concussion while tackling. During an early season football scrimmage, he tackled a player using the spearing technique. Immediately after the game was finished, he had an immediate, intense headache and vomited. There was no motor weakness, impaired sensation, or pain in his neck or upper limbs. Over the next few weeks, he had persistent bi-frontal headaches, radiating from the para-cervical area, usually aggravated by heavy lifting and straining. He had neck pain that was worse in the morning and exacerbated by flexion. Manual therapy helped relieve headaches and neck pain. He had multiple episodes of involuntary loss of stool that occurred in the act of passing gas. PHYSICAL EXAMINATION: Examination revealed moderate tenderness over the facet joints of C1-C2 and C2-C3 on the right side. Normal sensation, strength, and reflexes in the upper and lower limbs. There was full active, pain-free, range of motion with the neck. Spurling's maneuver was provocative of neck pain without radiation bilaterally. Cervical traction relieved his neck pain. Cranial nerves II-XII were normal. DIFFERENTIAL DIAGNOSIS: 1. Concussion with post-traumatic headache 2. Vertebro-basilar insufficiency 3. Cervical spinal cord neuropraxia TEST AND RESULTS: MRI cervical spine without contrast: Cervical vertebral body and disc space height, alignment, marrow signal, and spinal cord is normal. AP diameter of central canal measures 10 mm at C4-C5, while AP diameter of the central canal at C5 measures 16 mm. Torg ratio at C4-C5 measures 60% MRI/MRA Neck and Brain with and without contrast: Left-sided vertebral artery terminates as the left posterior inferior cerebellar artery. Right-sided vertebral artery is strongly dominant. Brain parenchyma is normal FINAL WORKING DIAGNOSIS: 1. Vertebro-basilar insufficiency 2. Cervical spinal stenosis and cord neuropraxia 3. Cervical facet arthropathy, C2-C3 TREATMENT AND OUTCOMES: 1. No clearance to return to football and contact sports. He is still experiencing cervicogenic headaches without a return to premorbid functional level. 2. Excluded neck manipulation and mobilization in treatment program, due to risk of occluding the one good vertebral artery. 3. Hyperbaric oxygen treatment transiently relieved headaches.

Eine ungewöhnliche Ursache für faziale Hypästhesie

A 58-year-old female admitted herself to the emergency department with progressive left-sided facial hypoesthesia. Magnetic resonance imaging revealed a 20 mm-sized aneurysm of the left vertebral artery leading to compression of the trigeminal nerve. An endovascular occlusion with a combined coiling and flow-diverter was performed. The left posterior inferior cerebellar artery (PICA) arised from the aneurysmal sac. Despite an extensive infarction of the left PICA-territory, the patient convalesced well and presented completely independent and without symptoms at the 4-week follow-up.

Delayed Endovascular Revascularization in a Patient With Progressive Neurological Deterioration From Bilateral Intracranial Vertebral Artery Occlusions: Case Report

This article describes delayed endovascular revascularization in a patient with clinical and radiographic evidence of posterior circulation hemodynamic failure in the setting of intracranial occlusive lesions. A 48-year-old man presented with a 6-week history of progressive headache, nausea, and ataxia. Bilateral intracranial vertebral artery occlusions and a left posterior inferior cerebellar artery stroke were diagnosed, and the patient began warfarin therapy. Despite these measures, the patient developed dense lower cranial neuropathies, including severe dysarthria, decreased left-sided hearing acuity, and left facial droop. He presented at this point for endovascular evaluation. The patient underwent successful revascularization with intravascular Wingspan stents (Boston Scientific, Natick, Massachusetts) in a delayed fashion (approximately 6 weeks after his initial stroke presentation). His neurological syndrome stabilized and began to improve slowly. Patients with arterial occlusion should be evaluated acutely for potential revascularization. In the posterior circulation, clinical progression may supplant physiological imaging in the assessment of hemodynamic collapse. A subpopulation of patients will present with progressive deficits distinct from extracranial manifestations of vertebrobasilar insufficiency; these patients should be considered for delayed revascularization.