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| Year : 2001 | Volume
: 49
| Issue : 4 | Page : 384-90 |
Vertebral artery dissection due to indirect neck trauma : an underrecognised entity.
Prabhakar S, Bhatia R, Khandelwal N, Lal V, Das CP
Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh - 160012, India.
Correspondence Address:
Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh - 160012, India.
[email protected]
Vertebral artery dissection is an important cause of brain stem stroke, especially in the young. Dissections of carotid and vertebral arteries in neck account for about 20% of strokes in young compared with 2.5% in the elderly. Three patients of vertebral artery dissection related to indirect neck trauma are described. The first patient developed the symptoms while dancing, the second after a trivial fall and the third while he was on a dental chair. None of them had a direct severe neck trauma or concomitant risk factor like hypertension, connective tissue disease or migraine. Clinical symptomatology was similar in all the patients and included occipito-nuchal pain, headache and brain stem dysfunction chiefly in the posterior inferior cerebellar artery (PICA) territory. One of the patients also had associated ischaemic myelopathy. MRA and DSA confirmed dissection in all with a predominant steno-occlusive picture. Cases of so called trivial neck movement/torsion related dissection have been described previously but have not received any major importance. Usually classified as 'spontaneous' or 'traumatic', there is a possible ambiguity in literature about appropriate terminology. We emphasise that a history of such subtle precipitating events be taken while diagnosing young patients with brain stem strokes, to recognise this clinical entity. Although mechanisms are not absolutely clear, yet there seems to be an important relationship between arterial dissection and neck movements or minor trauma.
How to cite this article:
Prabhakar S, Bhatia R, Khandelwal N, Lal V, Das C P. Vertebral artery dissection due to indirect neck trauma : an underrecognised entity. Neurol India 2001;49:384 |
How to cite this URL:
Prabhakar S, Bhatia R, Khandelwal N, Lal V, Das C P. Vertebral artery dissection due to indirect neck trauma : an underrecognised entity. Neurol India [serial online] 2001 [cited 2023 Mar 22];49:384. Available from: https://www.neurologyindia.com/text.asp?2001/49/4/384/1215 |
Dissection of cervical or cerebral arteries is important, albeit rare cause of stroke. Recently, this entity has received increased attention, possibly due to better diagnostic aids, as well as characterisation of typical symptoms and signs. Vertebral artery dissection is an important cause of brain stem ishaemia in young. Usually classified as 'spontaneous' or 'traumatic', cases related to trivial trauma have been frequently reported, although they have not received any major attention or classification. Three such cases are described, where a definite temporal correlation was present between neck movement, trivial trauma and acute arterial dissection. It is important to recognise and treat this syndrome because of a relatively benign course and potentially excellent outcome in most patients.
Case 1 : IM, 35 years old male, developed acute dizziness while dancing and moving his neck excessively at a friend's marriage, which settled in few minutes. One hour later, he developed severe headache, accompanied with nuchal pain and recurrent vomitings, lasting for few minutes. Next morning, the patient noticed dizziness and vertigo accompanied with sense of imbalance and a tendency to fall to his right. There was drooping of the right eyelid, awkward sensation on right half of face and swallowing difficulty. The patient was a non smoker, nondiabetic and a normotensive. Neurological examination revealed slurred speech, right Horner's syndrome, paresis of right V (sensory), VII, IX and X cranial nerves and right cerebellar signs. Motor examination was normal. Sensory examination revealed a crossed hemianaesthesia with involvement of face on the right side. Investigations of the patient revealed normal haemogram, renal function tests, lipidogram, coagulogram and APLA work up. ECG and echocardiography did not reveal any abnormality. MRI scan of the head revealed acute infarcts in the right cerebellar hemisphere, pons and medulla, chiefly in the PICA territory. MR angiogram revealed narrowing of proximal right vertebral artery with normal flow in mid part of the artery. There was complete occlusion of the vertebral artery beyond V3 segment [Figure - 1]. Transfemoral [digital] substraction angiogram (DSA) revealed irregular filling defect at V1 and V2 segments with narrowing and irregularity of the wall and complete occlusion at V3 segment. There was no filling of V4 segment of the vertebral or basilar artery. No evidence of aneurysm was seen. The patient received anticoagulation with warfarin for four months followed by aspirin prophylaxis. He made an excellent recovery over 2-3 weeks, and is presently completely independent with residual paraesthesias and numbness of right side of face.
Case 2 : MA, a BSF jawan, jumped from a height of 6 feet and fell down. There was no direct trauma to head, neck or back. Within few minutes, he developed occipitonuchal pain, severe vertigo, blurring of vision and diplopia. He had difficulty in balancing himself with a tendency to fall to the right and incoordination of right upper and lower limbs. There was accompanying facial asymmetry, decreased hearing from right side, difficulty in swallowing, and associated weakness of right side of body. This was an awkward sensation on left half of the body excluding
face. The patient was a healthy male with no preceding history of hypertension, diabetes or any chronic illness. He was a non-smoker and a nonalcoholic. Examination of the patient revealed a normal cardiovascular, chest and abdomen examination. CNS examination revealed a right sided Horner's syndrome, nystagmus to right, sensorineural type of hearing deficit in right ear and paresis of soft palate on right side. Motor examination revealed reduced tone and power in right sided limbs. Deep tendon reflexes were brisk on the right side and plantar response was extensor. Sensory examination revealed a crossed hemianaesthesia with involvement of the face on the right side. Investigations of the patient revealed a normal haemogram, coagulogram, lipid profile, APLA work up, EKG and echocardiogram. MRI head showed focal infarcts in superior vermis, right inferior cerebellar region, pons and right dorsal medulla [Figure - 3]. Focal hyperintensity was also noticed in right thalamic region. MR angiogram revealed a narrow right vertebral artery. There was disappearance of signals beyond the C2 vertebra along with suggestion of an intramural flap. Other vessels were normal. DSA [Figure. 4] revealed irregularity and narrowing of V3 segment of right vertebral artery with extension into the V4 segment. Filling of the PICA was normal. The patient received anticoagulation with warfarin for 3 months and was shifted to aspirin prophylaxis. He has made an excellent recovery and presently is only left with sensory dysfunction on left side of the body.
Case 3 : RS, 31 years male, went for a tooth extraction and was on the dental chair for more then 45 minutes. During the procedure, he developed sudden giddiness and vertigo, which lasted for few seconds. After about 2 hours, the patient had severe throbbing headache, accompanied by intense vomitings. Within few minutes, he noticed a sensation of reeling and inability to balance himself, with a tendency to fall. He also noticed weakness of left upper and lower limbs. The voice became low volume, and hoarse. He had difficulty in swallowing and nasal regurgitation of fluids. He was treated as a case of brainstem stroke at a private hospital. Four days later, he noticed difficulty in micturition in the form of hesitancy and increasing weakness of both lower limbs and left upper limb. There was decreased sensory perception below upper part of the chest. However, no fresh bulbar weakness was noticed. CNS examination revealed evidence of left Horner's syndrome, left V sensory, VII, IX and X nerve paresis, and bilateral gaze evoked nystagmus. Motor examination revealed grade 0/5 power in lower limbs and grade 4/5 in upper limbs. Deep tendon reflexes were attenuated in both lower limbs. All biochemical parameters, EKG and Echocardiography were normal. MRI head showed evidence of infarcts in left inferior vermis, pons and ventrolateral aspects of medulla. MRI of spine showed hyperintensity on T2WI in anterior part of the spinal cord from C4-D2 segments, suggestive of an infarct in T2WI [Figure. 5]. MRA [Figure. 6] showed drop in signal of left vertebral artery just beyond its origin till the formation of basilar artery. DSA confirmed the irregularity and narrowing of V2 segment with complete occlusion at the level of V3. No aneurysm was seen. He received heparin, followed by oral warfarin and intensive physiotherapy. The patient showed progressive improvement, and presently moves about with partial support. There is a residual spasticity in lower limbs, and urgency of micturition.
Arterial dissection is one of the many nonatherosclerotic vasculopathies that can cause brain ischaemia. Once considered rare and recognised only post-mortem, the credit for clarifying the symptomatology and delineating the physiology of this condition goes to Fisher and Mokri.[1] Vertebral artery dissection is an uncommon disorder with a variable reported frequency, and estimated annual incidence of approximately 1-1.5 cases per 10,000.[2] However, it is an important cause of posterior circulation ischaemia in young and middle aged patients and accounts for nearly one-fifth of such cases, compared to 2.5% in older patients,[3] although, the estimation of prevalence in elderly may be limited by co-existence of atherosclerosis as a confounding factor. Dissection of an artery occurs, when blood under pressure finds its way into the vessel wall, along a line of cleavage which is usually near the endothelial surface. It either leads to luminal narrowing and/or occlusion, if the tear is subintimal, or formation of a pseudoaneurysm with potential risk of bleeding if the dissection is subadventitial. Most cases of vertebral artery dissection are in the age group of 25-55 years, with a slight female preponderance.[4] All our patients were young males with a mean age of 32 years. Clinical symptomatology in our patients consisted of nuchal and/or head pain, which was followed by symptoms suggestive of brainstem ischaemia, predominantly in the distribution of PICA territory and simulating a lateral medullary syndrome. Associated features of AICA territory ischaemia and spinal cord infarction were also observed. In reported world literature, the symptomatology has been quite similar.[1],[3],[4],[5],[6],[7],[8],[9] Headache and neck pain are important warning symptoms of dissection with reported incidence of neck pain in half and headache in twothirds of patients. Pain often precedes neurological features by hours, days or rarely weeks.[2],[7] It usually starts suddenly, is sharp in quality and majority of time on the side of arterial dissection. Pain is possibly caused by excitation of nociceptors in the vessel wall as extracranial cerebral arteries are known to be pain sensitive. However, exact mechanisms are still elusive. Lateral medullary ischaemia has been seen in most of the patients, although involvement of thalamus and cerebral/cerebellar hemisphere is seen frequently.[2] Spinal cord infarction occurred in one of our patients, chiefly involving the cervical segment. Although uncommon, ischaemic myelopathy is being increasingly recognised as a complication of vertebral artery dissection.[10],[11] Both anterior and posterior spinal cord infarction have been described. Presentations with features of radiculopathy and focal motor deficits are also recognised.[10]
Pathophysiological mechanisms underlying neural damage following an arterial dissection may be diverse.[9] Stenosis or occlusion of the vertebral artery results in direct ischaemia of the brainstem or spinal cord. It may result from an intraluminal thrombus or by compression of the true lumen due to blood in the vessel wall.[12] Progressive thrombosis or artery to artery embolisation can cause distal ischaemia and branch artery occlusions.[1],[9],[12] The process can obstruct distal basilar artery flow, compress cranial nerves or cause a subarachnoid haemorrhage.[9] Spinal cord infarction is possibly related to hypoperfusion and watershed infarction, embolisation or anterior spinal artery occlusion.[10],[11]
Vertebral artery dissection is routinely labelled 'spontaneous' or 'traumatic', with cases related to minor, non-penetrating neck trauma or torsion placed inbetween the two. This classification is possibly ambiguous. A review of the literature on arterial dissections shower, then and in many so-called 'spontaneous' dissections, a history of abnormal neck movement, exercise or subtle trauma was present.[4],[5],[6],[7],[9],[12],[13],[14] In a recent Canadian survey,[14] 81% of dissections were associated with sudden neck movement ranging from therapeutic neck manipulation to a rigourous volleyball game, but some occurred during mild exertion such as lifting a pet dog or during a bout of coughing. Such causal potential trauma such as violent coughing, trampoline exercises, neck turning during a parade, basket ball game, dancing, swimming and minor falls have immediately antecedated the initial symptoms of dissection.[8],[9] Names like bottoms up' and 'beauty parlour' stroke have also been applied to such cases.[15] Chiropractic neck manouvers have been strongly associated with arterial dissection, with many cases reported in literature.[16],[17],[18] All our patients had a definite temporal correlation between onset of symptoms and preceding neck movements in two and a minor fall in the third. However, since the onset of dissection may precede the clinical symptoms by several hours or days, it might loosen the association between the two.[9] The distinction between spontaneous and movement related dissections seems more arbitrary and blurred when a post-resuscitation case is referred to as spontaneous and those occuring during backing -up of an automobile or swinging a baseball bat, as traumatic. The possible explanation of this causation is still not well defined. Authors have suggested the association of vertebral artery anomalies, tortousity, atherosclerosis as well as duration and force of the movement.[12] It is also likely that inherent vessel wall abnormalities predispose to dissection upon subtle trauma. Anatomically, the vertebral artery is divided into four arbitrary parts, designated V1 to V4. V1 extends from its origin to its entry into the foramen transversarium of the cervical vertebra. The entire length within the vertebral column is labelled as V2. V3 extends between its exit from the atlas upto its entry into the foramen magnum and the entire intracranial part is termed as V4. Most of the traumatic dissections involve the atlanto occipital segment. It is likely that increased mobility, poor anchoring into the neighbouring tissue and increased mechanical torsion and stretch at C1-C2 region predispose to mechanical injury.[8],[9],[15] This also explains the increased incidence of dissection along this segment during chiropractic manouvers. Reduction in vertebral artery blood flow during neck movements has been shown angiographically.[19],[20] Hyperextension of the neck has been considered as an important precipitating factor for occlusion and dissection, especially in the presence of vascular abnormalities and bony changes.[15] Aetiology usually remains obscure in most cases of spontaneous vertebral artery dissection. However, there does exist a striking discrepency between minor force and degree of arterial vulnerability, thereby suggesting an inherent disturbance in the vessel architecture, although the exact arteriopathy remains elusive.[21] Various predisposing conditions have been cited including fibromuscular dysplasia, hypertension and migraine etc. Recent infection[22] and hyperhomocystenaemia[23] have also been cited as potential risk factors. In our patients, we did not have a definite clinical or biochemical evidence for a potential underlying risk factor.
Diagnosis of this condition can be established by both non-invasive, and invasive means. Ultrasound examination of the neck vessels can suggest the presence of dissection, although the sensitivity to detect vertebral artery disease is low when compared with the carotids. However, duplex scans have been used to monitor healing of dissections and guide long term therapy.[1],[24],[25] Typical findings include increased arterial diameter, decreased pulsatility, intravascular abnormal echoes and haemodynamic evidence of decreased or reversed flow.[12] One of our patients underwent a dulpex scan which showed decreased systolic peak velocity, a smaller diastolic flow and some evidence of reversal, although no decrease in calibre or thrombus was seen. Magnetic resonance angiography (MRA) was performed in all three patients using time of flight (TOF) technique. This non-invasive technique is fast replacing conventional angiography as the gold standard in the diagnosis of dissections, with the advantage of showing the intramural flap and haematoma.[26],[27] Usual abnormalities observed are poor signals across the vessel, irregularity of vessel wall, aneurysmal dilatation, intimal flap, intramural haematoma or complete drop of signal beyond a level suggesting occlusion. All our patients showed poor signals, irregularity and occlusion of vertebral arteries suggestive of a steno-occlusive variety of dissection. The aneurysmal type of dissection was not encountered in any patient. All the patients had evidence of extracranial vertebral artery involvement. Long extent of dissection was seen in two of our patients. MRA is possibly the best technique to follow up the patients and monitor healing of dissections.[26],[27] It has been suggested that, in presence of a suspicious history, symptoms and signs of dissection, typical MRI findings of dissection, unusual location for atherosclerotic involvement and absence of coexisting atherosclerotic lesion, the diagnosis of arterial dissection may not be confirmed by a conventional angiogram.[27] Standard catheter angiography still remains the gold standard for diagnosis, as it allows excellent characterisation of the dissection.[1],[12] Usual features observed are irregularity and/or stenosis of the vessel, 'string sign' (arising as a result of a dissection that extends circumferentially around the lumen over a long segment), 'double lumen', pseudoaneurysm formation or complete occlusion.[6],[28] Stenosis is by far the commonest finding, being caused by a subintimal haematoma.[28] Digital substraction angiogram (DSA) through a transfemoral route was performed in all our patients. It revealed features of irregularity, stenosis and occlusion in all the three patients. Long extent of dissection was seen in two of our patients, with predominant involvement of V2 and V3 segments. Complete occlusion was seen at the C2 level in two patients (case 1 and 3). All patients chiefly had an extracranial vertebral artery involvement. In most reported studies in literature, V2-V3 segment of the vertebral artery is the commonest to be involved in dissections. None of the patients had bilateral involvement although reported incidence in spontaneous dissections is close to 50%, suggesting a possible predisposing arteriopathy. Management of this condition commonly involves anticoagulation with heparin followed by oral warfarin therapy, although no general agreement exists on the best management of this condition.[1],[3],[6],[12],[29] All our patients received low molecular weight heparin overlapped with warfarin in acute phase, and were later continued on oral warfarin for 3-4 months, followed by antiplatelet prophylaxis. Anticoagulation possibly aims at preventing thromboembolic complications, commonly seen to be associated with acute dissections. Some authors consider intradural extension of dissection as a contraindication for anticoagulation, because of risk of precipitating subarachnoid haemorrhage.[1] Although, conservative management of dissection presenting as SAH has been practiced, yet rebleeding is common and potentially fatal, making surgical intervention imperative and crucial for survival.[30] Endovascular treatment is usually practiced in centres equipped with intervention facilities. Surgical treatment of dissections, consisting of an in-situ interposition graft or extracranial - intracranial bypass, is indicated only for patients with persisting symptoms, refractory to maximal non-invasive management and who are not candidates for endovascular therapy.[29] Continuation of anticoagulation therapy may be guided by MRA or ultrasound. Persisting irregularity or stenosis at 3rd month necessitates continuation of therapy for another 3 months. If features of stenosis persist beyond 6 months, it is advisable to shift the patient on antiplatelet agents.[12] Overall prognosis of this clinical entity is good and encouraging, although factors like severity of ischaemic insult and extent of collateral flow do influence the overall outcome.[1] Nearly 75% of patients make excellent recovery and overall death rate is less than 5%. Almost 90% of the stenosis resolve, two-thirds of the occlusions are recanalised and one-third of aneurysms reduce in size.[1],[28] All the three cases reported here made an excellent recovery. Recovery was slow in one case with associated spinal cord infarction. Extracranial dissections hold a better prognosis than the intracranial ones, because risk of aneurysmal bleeds is much lower.[1],[5],[6],[12] Maximal improvement occurs in the first 3 months following a dissection. Risk of spontaneous dissection approximates 2% in the first month and decreases to about 1% per year.[31],[32] Dissection usually does not recur in the same vascular territory.[32]
It is worth realising that vertebral artery dissection is an important cause of posterior circulation stroke in young and middle aged adults. There seems to be an important association between neck movements and trivial neck torsion precipitating this condition, although controversies exist. However, it is important that patients, presenting with this clinical symptomatology are questioned in detail about precipitating factors. Whether the so called `spontaneous' dissections are truly spontaneous or effect of forgotten neck trauma is debatable. Still, many unanswered questions remain about this clinical entity and much remains to be learned about the pathogenesis and optimal treatment of this condition.
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