To describe a rare presentation of vertebral artery dissection (VAD) as a small but congruous incomplete homonymous hemianopia demonstrating use of visual field testing in the diagnosis.
A 30 year old woman had been unwell for 4 months with difficulty focusing, vertigo, dizziness and a feeling of falling to the right. A small but congruous right inferior homonymous quadrantanopia was found on examination leading to further investigation that uncovered a vertebral artery dissection and multiple posterior circulation infarctions including a left occipital stroke matching the field defect.
We describe an atypical case of VAD presenting with a small congruous quadrantanopia. This is a rare but significant condition that predisposes to multiple thromboembolic infarction that may be easily misdiagnosed and a high index of suspicion is required to make the diagnosis.
Vertebral artery dissection (VAD) associated with chiropractic cervical manipulation is a rare but potentially disabling condition. In this report, we present a young patient manifesting with repeated vertigo. Owing to the initial misdiagnosis, the patient later developed cerebellar stroke with inability to stand or walk. Vertigo and disequilibrium are the usual presenting symptoms of this condition, which can result from inner ear or vestibular nerve dysfunction, vertebrobasilar insufficiency, and even lethal cerebellar infarction or haemorrhage; these last two, although rarely seen in young adults, can be caused by traumatic or spontaneous arterial injury, including injury secondary to chiropractic cervical manipulation. A number of cases of VAD associated with chiropractic cervical manipulation have been reported, but rarely in the emergency medicine literature. We present a case of this rare occurrence, and discuss the diagnostic pitfalls.
vertebral artery dissection; manipulation
Vertigo is not an uncommon presentation to the emergency department. It is most commonly caused by benign peripheral processes, such as inner ear or vestibular nerve dysfunction, but can be due to central brain lesions. In this report, we present a central cause of isolated vertigo: brainstem infarct secondary to vertebral artery dissection (VAD). VAD is increasingly being recognised as an important cause of stroke in young people. We discuss the important features that need to be elicited to distinguish central from peripheral disease and the relevance of VAD.
Vertebral artery dissection (VAD) is an important cause of stroke in the young. VAD can present with a range of imaging findings. We sought to summarize the diagnostic value of various imaging findings in patients with symptomatic VAD.
We conducted a systematic review of observational studies, searching electronic databases (MEDLINE, EMBASE) for English-language manuscripts with >5 subjects with clinical or radiological features of VAD. Two independent reviewers selected studies for inclusion; a third adjudicated differences. Studies were assessed for methodological quality and imaging data were abstracted. Pooled proportions were calculated.
Of 3996 citations, we screened 511 manuscripts and selected 75 studies describing 1,972 VAD patients. Most studies utilized conventional angiography or magnetic resonance angiography (MRA) to diagnose VAD; CT angiography (CTA) and Doppler ultrasonography were described less frequently. Imaging findings reported were vertebral artery stenosis (51%), string and pearls (48%), arterial dilation (37%), arterial occlusion (36%), and pseudoaneurysm, double lumen, and intimal flap (22% each). In cases where conventional angiography was the reference standard, CTA was more sensitive (100%) than either MRA (77%) or Doppler ultrasonography (71%) (p=0.001).
Imaging findings vary widely in patients with VAD, with no single radiographic sign present in the majority of VAD patients. Non-specific radiographic signs predominate. CTA probably has greater sensitivity for dissection than MRA or ultrasound relative to conventional angiography. Higher quality studies on imaging techniques and radiographic criteria in subjects with VAD are needed. Future studies should compare imaging techniques in well-defined, undifferentiated populations of clinical VAD suspects.
vertebral artery dissection; neuroimaging; meta-analysis
Vertebral artery dissection (VAD) is an important cause of stroke in the young. It can present nonspecifically and may be misdiagnosed with adverse consequences. We assessed the frequency of head/neck pain, other neurological symptoms, and cerebrovascular events in symptomatic VAD.
We conducted a systematic review of observational studies, searching electronic databases (MEDLINE, EMBASE) for English-language manuscripts with >5 subjects with clinical or radiological features of VAD. Two independent reviewers selected studies for inclusion; a third adjudicated differences. Studies were assessed for methodological quality and clinical data were abstracted. Pooled proportions were calculated.
Of 3996 citations, we screened 511manuscripts and selected 75 studies describing 1,972 VAD patients. The most common symptoms were dizziness/vertigo (58%), headache (51%) and neck pain (46%). Stroke was common (63%), especially with extracranial dissections (66% vs. 32%, p<0.0001), while TIA (14%) and subarachnoid hemorrhage (SAH) (10%) were uncommon. SAH was seen only with intracranial dissections (57% vs. 0%, p=0.003). Fewer than half of the patients had obvious trauma, and only 7.9% had a known connective tissue disease. Outcome was good (modified Rankin scale (mRS) 0-1) in 67% and poor (mRS 5-6) in 10%.
VAD is associated with nonspecific symptoms such as dizziness, vertigo, headache, or neck pain. Ischemic stroke is the most common reported cerebrovascular complication. VAD should be considered in the diagnostic assessment of patients presenting with dizziness or craniocervical pain, even in the absence of other risk factors. Future studies should compare clinical findings as predictors in well-defined, undifferentiated populations of clinical VAD suspects.
vertebral artery dissection; dizziness; meta-analysis
Objectives: To define the natural history of spontaneous intracranial vertebral artery dissections (VADs) and to review current treatment strategies. Material and methods: We searched the MEDLINE database for all existing English and French literature on VADs through January 2008. Keywords employed were intradural/intracranial vertebral artery dissection, vertebral artery dissection, and vertebral artery dissection treatment. We also reviewed our series of patients with spontaneous VAD treated in the past 5 years. Data were collected, categorized, and analyzed. Results: In our sample of 457 patients, men were more frequently affected than women, and the mean age was 51.8 years. The majority of patients (79%) presented with subarachnoid hemorrhage (SAH). We experienced a high incidence (37%) of recurrent SAH, particularly within the first 24 hours after SAH first occurred. Angiographic fusiform dilatation and pearl-and-string lesions were the most common finding. Patients who presented with SAH fared worse than those who presented with ischemia. Conclusions: Due to a high rate of recurrent bleeding, we concluded that early treatment by either surgical or endovascular route is indicated in patients who present with SAH secondary to spontaneous intradural VADs. Treatment decisions should take into account the site and type of dissection, vertebral artery dominance, and involvement of posterior inferior cerebellar artery.
Vertebral artery; arterial dissection; intradural vertebral artery; vertebral artery dissection; vertebral artery dissection treatment
A 46-year-old male with juvenile myoclonic epilepsy was admitted to the neurological department for convulsive seizures just after lamotrigine was discontinued. On admission he was awake but had a right-sided hemiparesis with Babinski sign and ataxic finger-nose test on the left side. An MR scan showed a left-sided pontine infarction, an infarct in the left cerebellar hemisphere and a right vertebral artery dissection (VAD). The patient was treated with heparin and an oral anticoagulant for 6 months. Recovery of neurologic function was excellent. In patients with symptoms of disturbances of posterior circulation after epileptic seizures, VAD should be considered.
Seizure; Vertebral artery; Dissection; Stroke
Background and Purpose:
Multidetector computed tomography angiography (MDCTA) is a minimally invasive radiological technique providing high-resolution images of the arterial wall and angiographic images of the lumen. We studied the radiological features of vertebral artery dissection (VAD) in a consecutive series of patients investigated for acute stroke and subarachnoid hemorrhage (SAH) in order to confirm and define the diagnostic features of VAD on MDCTA.
Patients and Methods:
Review of patients identified prospectively over a 4-year period with VAD assessed by MDCTA was conducted. Radiological features of VAD on MDCTA were reanalyzed utilising previously reported criteria for VAD.
Thirty-five patients (25 males, mean age 49.6 years) with a total of 45 dissected vertebral arteries were reviewed. MDCTA features of VAD included increased wall thickness in 44/45 (97.7%) arteries and increased total vessel diameter in 42/45 arteries (93.3%). All dissected arteries had either lumen stenosis (21/45) or associated segmental occlusion (24/45). An intimal flap was detected in 6/45 (13.3 %) vessels. Twenty-five patients had follow-up imaging, 14/32 vessels returned to normal, 4 showed improvement in stenosis but did not return to normal and 14 demonstrated no change. The majority of non-occluded vessels became normal or displayed improved patency. Only 4/17 occluded arteries demonstrated re-establishment of flow. No adverse effects were recorded.
MDCTA is a safe and reliable technique for the diagnosis of VAD. Increased wall thickness (97.7%) and increased vessel wall diameter (93.3%) were the most frequently observed features.
Multidetector computed tomographic angiography; vertebral artery dissection; stroke; sub-arachnoid hemorrhage
This case report describes a transient ischaemic attack secondary to vertebral artery dissection (VAD) in a young male body builder. This occurred following weight training with weights across the back and shoulders. The patient was also known to take multiple performance enhancing agents including anabolic steroids, slimming agents, stimulants and human growth hormone. Cases of VAD have been described with cervical manipulation in the past and an association between the use of anabolic steroids and embolic strokes has been described. To the authors knowledge, this is the first case describing a link between VAD, weight training and anabolic steroids.
The understanding of the relationship between cervical manipulative therapy (CMT) and vertebral artery dissection and stroke (VADS) has evolved considerably over the years. In the beginning the relationship was seen as simple cause-effect, in which CMT was seen to cause VADS in certain susceptible individuals. This was perceived as extremely rare by chiropractic physicians, but as far more common by neurologists and others. Recent evidence has clarified the relationship considerably, and suggests that the relationship is not causal, but that patients with VADS often have initial symptoms which cause them to seek care from a chiropractic physician and have a stroke some time after, independent of the chiropractic visit.
This new understanding has shifted the focus for the chiropractic physician from one of attempting to "screen" for "risk of complication to manipulation" to one of recognizing the patient who may be having VADS so that early diagnosis and intervention can be pursued. In addition, this new understanding presents the chiropractic profession with an opportunity to change the conversation about CMT and VADS by taking a proactive, public health approach to this uncommon but potentially devastating disorder.
Herein, we report a successful bridge to heart transplantation by use of the TandemHeart® percutaneous ventricular assist device (pVAD) in a chronic aortic dissection patient who was experiencing postcardiotomy shock. The patient had undergone an aortocoronary bypass to treat an acute, extensive myocardial infarction that had resulted from severe stenosis of a Cabrol-like graft to the left main coronary artery. The TandemHeart was used successfully, despite classic contraindications for pVAD support. The outcome shows that, in critically ill cardiogenic shock patients, a permissive approach to pVAD use is valuable in screening candidates for long-term ventricular assist device support or for heart transplantation. This case also reveals the validity of direct bridging to transplantation from a pVAD in carefully selected patients.
Aneurysm, dissecting; aortic aneurysm/mortality/surgery; cardiac output/physiology; heart transplantation; heart-assist devices; myocardial infarction/etiology; postoperative complications; shock, cardiogenic/therapy; treatment outcome; ventricular dysfunction, left/physiopathology/therapy
A 36-year-old man presented a sudden left occipital headache and right limb weakness after tooth-brushing. Conventional catheter digital subtraction angiography (DSA) showed a left VA occlusion at the crotch of the posterior inferior cerebellar artery. Four days later, the patient got worse. The angiogram showed the left vertebral artery had reopened and the basilar trunk occluded above the AICA. He died two days later and autopsy demonstrated a dissection of the basilar arteries. Based on the autopsy data from the patient in this study, we suggest that the BA dissection might be due to left VA dissection, and placing a stent on the juncture between the uninjured VA and the basilar trunk might be an effective method to prevent fatal BA occlusion.
cerebral infarction, diagnosis, treatment, vertebral arterial dissection
Phospholipase A2 (PLA2), cyclooxygenase (COX) and prostaglandin (PG) synthase are enzymes involved in arachidonate cascade. PLA2 liberates arachidonic acid (AA) from cell membrane lipids. COX oxidizes AA to PGG2 followed by an endoperoxidase reaction that converts PGG2 into PGH2. PGs are generated from astrocytes, microglial cells and neurons in the central nervous system, and are altered in the brain of demented patients. Dementia is principally diagnosed into Alzheimer’s disease (AD) and vascular dementia (VaD). In older patients, the brain lesions associated with each pathological process often occur together. Regional brain microvascular abnormalities appear before cognitive decline and neurodegeneration. The coexistence of AD and VaD pathology is often termed mixed dementia. AD and VaD brain lesions interact in important ways to decline cognition, suggesting common pathways of the two neurological diseases. Arachidonate cascade is one of the converged intracellular signal transductions between AD and VaD. PLA2 from mammalian sources are classified as secreted (sPLA2), Ca2+-dependent, cytosolic (cPLA2) and Ca2+-independent cytosolic PLA2 (iPLA2). PLA2 activity can be regulated by calcium, by phosphorylation, and by agonists binding to G-protein-coupled receptors. cPLA2 is upregulalted in AD, but iPLA2 is downregulated. On the other hand, sPLA2 is increased in animal models for VaD. COX-2 is induced and PGD2 are elevated in both AD and VaD. This review presents evidences for central roles of PLA2s, COXs and PGs in the dementia.
Alzheimer’s disease; arachidonic acid; cyclooxygenase; mixed dementia; phospholipase A2; prostaglandin; vascular dementia; PGD2; 15d-Δ12,14-PGJ2
Spinal manifestations of vertebral artery dissection (VAD) are rare events and are typically symptomatic with neck pain and ischemic brain injury. We report a patient presenting with unusual peripheral paresis of the right upper limb due to an intramural hematoma of the right vertebral artery with local compression of C5 and C6 as the cause of cervical radiculopathy. These symptoms completely resolved after anticoagulation and physical therapy.
When a tear occurs in one of the major cervicocerebral arteries and allows blood to enter the wall of the artery and split its layers, the result is either stenosis or aneurysmal dilatation of the vessel. Vertebral artery dissection (VAD) is an infrequent occurrence but is a leading cause of stroke in young and otherwise healthy patients. This article discusses recent developments in understanding of the epidemiology and pathogenesis of VAD and the various clinical manifestations, methods of diagnosis, and approaches to treatment.
Stenosis; Aneurysmal dilatation; Vertebral artery dissection; Diagnosis; Treatment
Intracranial vertebral artery dissection (VAD) represents the underlying etiology in a significant percentage of posterior circulation ischemic strokes and subarachnoid hemorrhages. These lesions are particularly challenging in their diagnosis, management, and in the prediction of long-term outcome. Advances in the understanding of underlying processes leading to dissection, as well as the evolution of modern imaging techniques are discussed. The data pertaining to medical management of intracranial VADs, with emphasis on anticoagulants and antiplatelet agents, is reviewed. Surgical intervention is discussed, including, the selection of operative candidates, open and endovascular procedures, and potential complications. The evolution of endovascular technology and techniques is highlighted.
intracranial, vertebral artery, stroke, hemorrhage, subarachnoid, dissection, dissecting aneurysm, pseudoaneurysm, surgery, endovascular, stent
Cholinergic stimulation of dopamine neurons in the ventral tegmental area (VTA) underlies activation of the brain reward circuitry. Activation of this circuit is proposed to preferentially suppress the affective reaction to noxious stimulation. Vocalization afterdischarges (VADs) are a validated model of the affective response of rats to noxious tailshock. The antinociceptive action of the acetylcholine agonist carbachol microinjected into the VTA on VAD threshold was compared to its effect on the thresholds of other tailshock-elicited responses (VDS = vocalizations during shock, and SMR = spinal motor reflexes). Whereas VADs are organized within the forebrain, VDSs and SMRs are organized at medullary and spinal levels of the neuraxis, respectively. Carbachol (1 μg, 2 μg, and 4 μg) injected into VTA produced dose-dependent increases in VAD and VDS thresholds, although increases in VAD threshold were significantly greater than increases in VDS threshold. Administration of carbachol into VTA failed to elevate SMR threshold. Elevations in vocalization thresholds produced by intra-VTA carbachol were reversed in a dose-dependent manner by local administration of the muscarinic receptor antagonist atropine sulfate (30 μg and 60 μg). These results provide the first demonstration of the involvement of the VTA in muscarinic-induced suppression of pain affect.
Cholinergic activation of the brain reward circuit produced a preferential suppression of rats’ affective reaction to noxious stimulation. The neurobiology that relates reinforcement to suppression of pain affect may provide insights into new treatments for pain and its associated affective disorders.
The study of fungal regulatory networks is essential to the understanding of how these pathogens respond to host environmental signals with effective virulence-associated traits. In this study, a virulence-associated DEAD-box RNA helicase–encoding gene (VAD1) was isolated from a mutant defective in the virulence factor laccase. A Δvad1 mutant exhibited a profound reduction in virulence in a mouse model that was restored after reconstitution with WT VAD1. Loss of VAD1 resulted in upregulation of NOT1, a gene encoding a global repressor of transcription. NOT1 was found to act as an intermediary transcriptional repressor of laccase. Vad1 was located within macromolecular complexes that formed cytoplasmic granular bodies in mature cells and during infection of mouse brain. In addition, VAD1 was shown by in situ hybridization to be expressed in the brain of an AIDS patient coinfected with C. neoformans. To understand the role of VAD1 in virulence, a functional genomics approach was used to identify 3 additional virulence determinants dependent on VAD1: PCK1, TUF1, and MPF3, involved in gluconeogenesis, mitochondrial protein synthesis, and cell wall integrity, respectively. These data show that fungal virulence-associated genes are coordinately regulated and that an analysis of such transcriptomes allows for the identification of important new genes involved in the normal growth and virulence of fungal pathogens.
Bowhunter's syndrome, also known as rotational occlusion of the vertebral artery, involves posterior circulation ischemia resulting from dynamic compromise of the dominant vertebral artery. This case highlights the importance of provocative digital subtraction angiography in making the diagnosis. A 41-year-old man presented for outpatient neurological evaluation for “lightheadedness” of several years' duration provoked by leftward head rotation. The only abnormality identified on initial magnetic resonance angiography was atresia of the nondominant left vertebral artery. Conventional digital subtraction angiography (DSA) followed by provocative DSA revealed development of a dynamic stenosis of the right vertebral artery involving the extraforaminal segment just superior to the C1 vertebra. Noncontrast computed tomography of the cervical spine confirmed ossification of the posterior right atlanto-occipital membrane leading to a near complete bony arcuate foramen. Following neurosurgical decompression, the patient demonstrated complete resolution of all neurologic symptoms. Bowhunter's syndrome is a unique clinical entity that must be considered in the evaluation of patients with symptoms of posterior circulation ischemia. Provocative DSA remains the preferred modality for definitive diagnosis.
Spontaneous coronary artery dissection and vertebral artery dissection are rare, life-threatening conditions. The pathophysiology of spontaneous coronary artery dissection during the peripartum period is poorly understood. We present a case of spontaneous multivessel dissection in a 32-year-old postpartum woman who presented with neck and chest pain. The patient's coronary and vertebral artery dissections were diagnosed with use of multiple imaging methods, and dissection of the internal mammary artery was discovered during surgery. The patient underwent successful coronary artery bypass grafting and remained asymptomatic 2 years later. To our knowledge, this is the first report of simultaneous coronary, vertebral, and internal mammary artery dissection in a postpartum woman. Early recognition and treatment is crucial, given the high mortality rate associated with spontaneous dissection.
Acute coronary syndrome/etiology; coronary artery bypass; postpartum period; pregnancy complications, cardiovascular/diagnosis; rupture, spontaneous/diagnosis/etiology/surgery; treatment outcome; vertebral artery dissection/epidemiology/surgery/ultrasonography
It is generally accepted that patients who require biventricular mechanical support (BiVAD) have poorer outcomes than those requiring isolated left ventricular support (LVAD). However, it is unknown how the timing of BiVAD insertion affects outcomes. We hypothesized that planned BiVAD insertion improves survival compared to delayed conversion of LVAD to BiVAD.
We reviewed and compared outcomes of 266 patients undergoing LVAD or BiVAD placement at the University of Pennsylvania from April 1995 to June 2007. We subdivided BiVAD patients into planned BiVAD (P-BiVAD) and delayed BiVAD (D-BiVAD) groups, based on the timing of RVAD insertion. We defined D-BiVAD as any failure of isolated LVAD support.
Of 266 LVAD patients, 99 required BiVAD (37%). We compared preoperative characteristics, successful bridging to transplant, survival to hospital discharge, and Kaplan-Meier one-year survival between P-BiVAD (n=71) and D-BiVAD (n=28) groups. Preoperative comparison showed that patients who ultimately require biventricular support have similar preoperative status. LVAD (n=167) outcomes in all categories exceeded both P-BiVAD and D-BiVAD outcomes. Further, P-BiVAD patients had superior survival to discharge than D-BiVAD patients (51% v 29% p<0.05). One-year and long-term Kaplan-Meier survival distribution confirmed this finding. There was also a trend towards improved bridging to transplant in P-BiVAD (n=55) vs. D-BiVAD (n=22) patients (65% v 45% p=0.10).
When patients at risk for isolated LVAD support failure are identified, proceeding directly to BiVAD implantation is advised, as early institution of biventricular support results in dramatic improvement in survival.
Several population based studies have demonstrated an association between hypo-or hyperthyroidism and dementia in last two decades. As a consequence, thyroid stimulating hormone has become part of the screening laboratory test for dementia.
The aim of the present study was to evaluate the association between thyroid function and Alzheimer's disease (AD) and vascular dementia (VaD) and to determine the risk of AD and VaD in clinically euthyroid patients.
Materials and Methods:
A cross-sectional hospital based study was carried out in subjects diagnosed with AD/VaD and were assessed for thyroid status as routine screening test.
Free T3, free T4 and TSH were studied in 114 AD patients (mean age: 65 years), 35 VaD patients (mean age: 62 years) and 105 control subjects (mean age: 62 years). In AD group, TSH levels were significantly lower than controls (P = 0.00) and for each unit increase in TSH level, the odds of having dementia decreased by 37.1%. No such relation was seen in VaD.
The results suggest a consistent association of subclinical hyperthyroidism and AD.
Alzheimer's disease; Dementia; thyroid status; thyroid stimulating hormone; vascular dementia
The objective of this study was to compare the occurrence and severity of behavioral and psychological symptoms of dementia (BPSD) between vascular dementia (VaD) and vascular cognitive impairment-no dementia (VCI-ND).
Materials and Methods:
Consecutive patients presenting with cognitive impairment at least 3 months after an ischemic stroke and with a Hachinski Ischemic Score ≥4 were included. VaD was diagnosed as per National Institute of Neurological Disorders and Stroke – Association Internationale pour la Recherche et l’Enseignement en Neurosciences criteria for probable VaD and VCI-ND on the lines of the Canadian study of health and aging. The severity of cognitive impairment and the behavioral/psychological symptoms were studied by means of the clinical dementia rating scale and the neuropsychiatric inventory (NPI) respectively.
All patients with VaD and 89% of those with VCI-ND had at least one BPSD. The mean no. of symptoms per patient and the total NPI scores were higher in VaD than in VCI-ND. Apathy and night-time behavior disturbances were significantly more common and severe in VaD.
BPSD are very common both in VCI-ND and in VaD. The profile of BPSD is similar in both groups, albeit more severe in VaD. The net burden of BPSD is higher in VaD as compared to VCI-ND.
Behavioral and psychological symptoms; neuropsychiatric inventory; vascular cognitive impairment; vascular cognitive impairment-no dementia; vascular dementia
The diagnosis of vascular dementia (VaD) describes a group of various vessel disorders with different types of vascular lesions that finally contribute to the development of dementia. Most common forms of VaD in the elderly brain are subcortical vascular encephalopathy, strategic infarct dementia, and the multi infarct encephalopathy. Hereditary forms of VaD are rare. Most common is the cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Sporadic forms of VaD are caused by degenerative vessel disorders such as atherosclerosis, small vessel disease (SVD) including small vessel arteriosclerosis, arteriolosclerosis, and lipohyalinosis, and cerebral amyloid angiopathy (CAA). Less frequently inflammatory vessel disorders and tumor-associated vessel lesions (e.g. angiocentric T-cell or angiotropic large cell lymphoma) can cause symptoms of dementia. Here, we review and discuss the impact of vessel disorders to distinct vascular brain tissue lesions and to the development of dementia in elderly individuals. The impact of coexisting neurodegenerative pathology in the elderly brain to VaD as well as the correlation between SVD and CAA expansion in the brain parenchyma with that of Alzheimer’s disease (AD)-related pathology is highlighted. We conclude that “pure” VaD is rare and most frequently caused by infarctions. However, there is a significant contribution of vascular lesions and vessel pathology to the development of dementia that may go beyond tissue damage due to vascular lesions. Insufficient blood blow and alterations of the perivascular drainage mechanisms of the brain may also lead to a reduced protein clearance from extracellular space and subsequent increase of proteins in the brain parenchyma, such as the amyloid β-protein, and foster, thereby, the development of AD-related neurodegeneration. As such, it seems to be important for clinical practice to consider treatment of potentially coexisting AD pathology in cognitively impaired patients with vascular lesions.
Atherosclerosis; small vessel disease; cerebral amyloid angiopathy; dementia; neurodegeneration; perivascular drainage
Traumatic intracranial vertebral artery injury is a relatively rare but potentially fatal disease. We present a case of a 63-year-old man who presented with sudden onset of loss of consciousness after hitting his head. After immediate resuscitation, he showed quadriplegia and absence of spontaneous breathing. Brain and cervical spine magnetic resonance imaging revealed an atlantoaxial subluxation, fractured C2 odontoid process, left vertebral artery occlusion, and bilateral extensive ischemia in the medulla oblongata and high cervical spinal cord. Digital subtraction angiography demonstrated left vertebral artery dissection just below the level of vertebral body C2.
vertebral artery dissection; brainstem infarction; bilateral spinal cord infarction; neck trauma