VAD CASE 1 - Introduction
The patient was a 29-year-old woman with a history of migraine headaches who has otherwise been in good health. She stated that earlier today she was walking in her house and talking on the phone when suddenly she started staggering to her right and fell onto her couch. She stated that when she was lying on the couch and tried to focus on things, the room was spinning and she could not make her eyes focus. She had no nausea, diaphoresis, or vomiting. She noticed no other complaints or deficits. After approximately one to two minutes, the feeling of spinning went away and the patient stated that she has had no recurrence. The only other thing she notes is that since the episode, she has a pain going up the left side of her neck and into the left side of her head. She states that this is not severe. She says that her migraines are usually in the frontal area or behind either eye. She has never had a migraine with similar symptoms in the past. Past medical history was significant for migraine headaches. Current medications were oral contraceptives and Imitrex prn. Patient doesn't smoke cigarettes or drink alcohol. She is a housewife and mother of two children. Family history is unremarkable.
Upon physical exam: BP: 137/88, Pulse: 80, Respiratory rate: 14. The pupils were equally round and reactive. Extraocular movements were intact. The neck was supple and non-tender to palpation and she had no pain on range of motion. There were no bruits auscultated in the neck. Cardiac examination was normal with regular rate and rhythm and no murmurs. Neurological examination showed no focal deficits. Sensation was intact and deep tendon reflexes were 2 + and equal bilaterally. Toes were down going and the gate was normal. Heel-toe walking was normal. There was no dysmetria.
Medical decision making: With the history of an unexplained episode of vertigo and left neck pain it was felt that vertebral artery dissection should be ruled out. The patient was given one aspirin while in the emergency department and magnetic resonance angiography was arranged. Magnetic resonance angiography showed a diminutive left vertebral artery with a focal area of absent/decreased flow and abnormal signal hyperintensity from the C1-2 through the C5-6 levels. These findings likely represent dissection of a short segment of vertebral artery.
Extracranial cerebral arterial dissections occur when there is a tear in the intima of the blood vessel allowing blood to dissect in the wall of the artery. Neurological sequelae can result from this in one of two ways:
- The extramural hematoma may compromise the lumen of the blood vessel reducing flow to the affected part of the brain.
- There may be thrombus formation at the site of the dissection which can either locally occlude the blood vessel or cause an artery to artery embolus to a more distal intracerebral artery.
Arterial dissections may occur spontaneously or may be associated with trauma. The magnitude of the trauma may be quite trivial such as turning the head or looking upwards. Dissections may involve either the carotid or vertebral arteries. The most typical location for either carotid or vertebral dissections is at the C1-2 level.
Carotid arterial dissections are more frequently reported than vertebral dissections. Carotid dissections may account for as many as 2.5% of all strokes. Seventy per cent of the patients are between the ages 35 and 50 with a mean age of 44 years. Although there is a slight predilection for females in vertebral artery dissection, carotid artery dissections occur equally in males and females. Patients with carotid or vertebral artery dissection may have an underlying arteriopathy.
The major presenting features are typically stroke or transient ischemic attack associated with pain in the ipsilateral neck, face or head. With carotid dissection, an ipsilateral Horner's syndrome will occur in 40% of patients. Headache or neck pain will often precede the onset of ischemic symptoms by hours to days. Neck pain is present in only 21% of patients with carotid dissection but over 50% of patients with vertebral dissection. Headache is present in about 60% of each. Arterial dissections occur more frequently in patients with a history of migraine, although typically the headache experienced at the time of the dissection is not migraine-like.
The key to diagnosing arterial dissection is suspecting the disease. Evaluation should be undertaken in any patient who presents with neurologic signs or symptoms of stroke/TIA with associated neck pain or headache. Patients with a history of arteriopathy (Marfan's, Ehlers-Danlos, etc.) should be highly suspect. Also, a history of neck trauma, even relatively trivial, should raise the index of suspicion.
The best non-invasive test for diagnosing arterial dissection is magnetic resonance angiography. If the diagnosis is suspect on MRA/MRI, angiography may be needed to confirm the diagnosis. In many cases MRI/MRA alone is sufficient to establish the diagnose. If MRA/MRI or angiography is not immediately available, carotid duplex scanning may be useful in diagnosing a carotid artery dissection. Duplex scanning may be valuable in diagnosing vertebral artery dissection with experienced operators.
In patients who present with ischemic stroke or TIA symptoms, one should obtain non-contrast cranial CT as the initial test.
There are no randomized controlled trials of the management of extracranial artery dissection. Because the symptoms or sequelae of dissection are related to thrombosis and/or embolus, anticoagulation is the main stay for treatment. A patient with a documented vertebral or carotid artery dissection should be given intravenous heparin and then switched to warfarin anticoagulation. Some physicians might opt for anti-platelet therapy alone which may be quite adequate. As mentioned, there are no randomized-controlled trials to establish the superiority of one treatment over another.
Re-imaging is usually done in three to six months. After the artery appears normal on MRA or angiography, anticoagulation or anti-platelet therapy can be discontinued. There is an incidence of recurrent dissection which is approximately 3% for carotids and 5% for vertebral artery dissections.
The patient was admitted to the Neurology inpatient service and started on intravenous heparin. On hospital day two, the patient was begun on Coumadin to achieve an INR of 2-3. This was achieved after several days and the patient was discharged from the hospital. As an outpatient she underwent evaluation by Medical Genetics for Ehler-Danlos Type 4 syndrome, which was negative. The Medical Genetics service felt that there was no indication that the patient had any underlying arteriopathy or connective tissue disorder. Six months later, the patient had repeat magnetic resonance angiography which showed normalization of the MR angiographic appearance of the left vertebral artery since the prior examination. The MR was read as normal. The patient was discontinued from the Coumadin and has remained well.
VAD CASE 2
Lethal Vertebral Artery Dissection in Pregnancy:
A Case Report and Review of the Literature
A 39-year-old woman in her 39th week of pregnancy had been discovered apneic and unresponsive at home approximately 1.5 hours after she had complained of shortness of breath and headache. She had a past medical history of asthma. No other significant symptoms were reported by the family members. On the scene, the emergency medical services team had found the patient cyanotic, unresponsive, apneic, and in asystole with 4-mm fixed pupils. Resuscitative measures at the scene included intubation, intravenous fluid, bolus epinephrine administration, and cardiopulmonary resuscitation.
The patient arrived at the emergency department still in asystole. Atropine and intracardiac epinephrine were given and bilateral needle thoracostomies were performed to relieve possible tension pneumothorax. Because all resuscitative measures were without effect, emergency cesarean section was performed and a viable female infant was delivered. The mother was pronounced dead immediately thereafter. Complete autopsy was performed the next day.
Examination of the central nervous system revealed the presence of a large SAH at the base of the brain. The hemorrhage was located near the circle of Willis and extended into the fourth ventricle, slightly displacing the brainstem and symmetrically extending through the Sylvian fissure to cover the hippocampi, superior surfaces of temporal lobes and lateral bases of the frontal lobes, the occiput, and virtually the entire surface of the cerebellum. No aneurysms were identified during in situ examination or following dissection of the circle of Willis and the proximal branches from the base of the brain; however, asymmetry in the diameters of the vertebral arteries was noted. Gross examination of the right vertebral artery showed hemorrhage within the adventitia. Acute dissection and rupture of the artery were diagnosed by microscopic examination. The inflammatory reaction to arterial necrosis included a locally intense neutrophilic infiltrate with early leukocytoclasis, indicative of likely onset of dissection 1 to 2 days prior to death. Other significant findings at autopsy were renal glomerular and tubular abnormalities consistent with pre-eclampsia and hepatic steatosis. No left ventricular hypertrophy or other changes consistent with chronic hypertension were present.
To our knowledge, this is the first case to report vertebral artery dissection as a cause of lethal SAH during pregnancy. Previously reported cases of vertebral artery dissection occurring during pregnancy have all involved medical treatment, with favorable outcome for both mother and baby. Histopathologic features of the dissection in our case were consistent with onset 1 to 2 days prior to death. The patient's apparent delay in recognizing or reporting symptoms in our case may underlie its lethal outcome.
The incidence of SAH is stable, at approximately 6 cases per 100,000 patient years. Case fatality is 50% overall. Subarachnoid hemorrhage in pregnancy is uncommon and has a high associated mortality. Pre-eclampsia may be a contributing factor because it has been linked to SAH and because hypertension is a risk factor for arterial dissection. An increase in intravascular volume, anatomic predisposition, and hormone-induced changes of the vascular wall integrity also are factors associated with pregnancy that have been proposed as predisposing to arterial dissection. Vertebral artery dissection has been described following chiropractic manipulation, yoga, exercise, violent cough, or rapid head turning. Excessive contralateral head rotation compresses the carotid or vertebral artery against bony structures, causing intimal tears and creating a lesion that gives rise to dissection. Predisposing conditions for development of arterial dissections also include chronic hypertension, Marfan syndrome, fibromuscular dysplasia, vasculitis, and cystic medial necrosis, None of these factors were identified in our case.
The proportion of all SAH cases that arise from a dissected vertebral artery is not known with certainty, but it is small. In a postmortem study of fatal SAH, dissection was found in 5 of 110 patients. The most common cause of SAH is rupture of a congenital saccular (berry) aneurysm, which occurs in 85% of identified cases. Idiopathic perimesencephalic hemorrhages are the next most common cause (10% of cases), and usually are associated with a history of hypertension. Other miscellaneous causes of SAH together account for the remaining approximately 5% of cases. Arterial dissection, in general, tends to be recognized more often in the carotid than in the vertebral artery; however, SAH secondary to arterial dissection occurs mostly with vertebral artery involvement.
Unilateral vertebral artery dissections may go unrecognized because of collateral circulation. Dissection may occur at any point along the course of the vertebral artery but it is most frequent in its distal end. Arterial compromise can result in brain injury by several mechanisms; therefore, signs and symptoms of vertebral artery dissection are diverse. Neck or occipital pain usually precedes symptoms of brain ischemia. Neurologic deficits that may accompany SAH from vertebral artery dissection are palsies of the ninth and tenth cranial nerves, secondary to subadventitial dissection or Wallenberg syndrome. The patient in our case apparently had no neurologic symptoms besides headache, despite autopsy findings suggesting occurrence of the dissection at least 24 hours prior to death.
In summary, we report the first case of spontaneous right vertebral artery dissection with secondary SAH with a fatal outcome. Only 2 cases of vertebral artery dissection associated with pregnancy or peripartum period have been reported. Both previously reported cases had a favorable outcome with medical management. The lethal outcome in our case may have been related to absent or ignored clinical symptoms.
Madalina Tuluc, MD; Daniel Brown, MD; Bruce Goldman, MD
VAD CASE 3
Vertebral Arterial Dissection Caused by Chiropractic Treatment
A 37-year-old man sought chiropractic treatment for a persistent bitemporal headache of four weeks' duration. On history, the headache seemed to be of muscular tension type. The patient had previously been well, with no history hypertension, diabetes or neck trauma. He smoked 20 cigarettes daily, drank little alcohol, took no regular medications, and had no relevant family history.
Immediate following his first cervical manipulation, while still in the chiropractor's rooms, he reported severe diplopia, dysarthria and
ataxia. He sat in the waiting room for an hour before driving back to his office; he was not advised to seek a medical opinion. The symptoms worsened, and a colleague drove him home, where he slept. On waking, he had only mild headache.
Two days later, the patient presented to hospital with severe ataxia, nausea and vomiting, and complaining of vertigo, diplopia and right-sided neck pain. He was afebrile had a pulse rate of 88 bpm and a blood pressure of 130/80 mmHg. He had no heart bruits or murmurs, and was alert and oriented. His pupils were equal and reactive, with normal fundi. Nystagmus and diplopia were present bilaterally, but more pronounced on right gaze.
He had a profound right sensorineural hearing loss (confirmed by audiometry). The other cranial nerves were normal. Ataxia was predominantly right-sided, with upper-limb past pointing, intention tremor, poor heel-shin coordination, 'ataxic wide-based gait, and a tendency to fall to the right. Tone and power were essentially normal bilaterally, with symmetrical deep tendon reflexes
and downgoing plantar responses.
Dissection of vertebral artery with emboli was suspected. Cerebral CT scan suggested a right brainstem infarct, and the patient was
commenced on intravenous heparin. Routine blood tests, electrocardiogram and chest films were unremarkable (apart from a cholesterol level of 6.0 mmol/L [normal range, 3.9-5.5 mmol/L] and triglyceride level of 2.79 mmol/L [normal range, 0.5-1.7 mmol/LI). An MR1 scan five days after presentation showed multiple infarcts within the deep white matter of both cerebellar
hemispheres, and a well defined, wedge-shaped infarct of the inferior aspect of the right cerebellar hemisphere, with involvement of the adjacent portion of the right middle cerebellar peduncle without appreciable mass effect (Figure 2).
Axial scans demonstrated high signal strength in the vessel wall consistent with mural thrombus. Magnetic resonance angiography demonstrated a patent right VA, but there was minimal to no filling of the left VA for virtually its entire extracranial course (Figure 3). Appearances were consistent with a left VAD, a large right anterior inferior cerebellar artery territory infarct, and several smaller infarcts in the superior cerebellar artery territory.
The symptoms of vertigo, nausea and vomiting settled quickly, with residual diplopia, hearing impairment and rightsided limb and gait ataxia. Following initial physiotherapy, occupational therapy and alternate eye patching, the patient was transferred for rehabilitation. At outpatient review one month later, he was mildly ataxic, with right-sided past pointing and intention tremor. During the following six months, his symptoms resolved further but the diplopia and ataxia failed to resolve.
"Is it true that getting your neck adjusted by a chiropractor can actually cause a stroke?" - "Absolutely"
Sandy Nette's Story
One of Britt's goals is that chiropractors be required to offer an informed consent form.
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