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Spontaneous internal carotid artery dissection (sICAD) is an uncommon cause of isolated cranial nerve palsies. Commonly patients present with stroke, headache, facial pain and Horner's syndrome, with upto 16% having cranial nerve palsies. We present the case of a 55-year-old man who presented with hoarseness, dysphagia and tongue swelling, mimickin...
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Purpose
Especially in acute onset of ophthalmoplegia, efficient neuroradiological evaluation is necessary to assist differential diagnosis, clinical course, and treatment options.
Methods
Different manifestations of ophthalmoplegia are explained and illustrated by characteristic neuroradiological and clinical findings.
Results
To present those op...
Citations
... In the literature, isolated palsies of CN II, III, VII, IX, X, and XII have been reported, while CN XI palsy only occurs in combination with other caudal CN palsies (Tables 1, 2). In view of the available literature, these palsies originate either from an expansive vessel wall hematoma causing a local mass effect on adjacent structures or as a consequence of peripheral nerve ischemia (i.e., microembolism or hypoperfusion of vasa nervorum) (36,54,62,87). In cases where isolated CN palsies occur due to sCeAD, the available data depicted in Table 1 support such hypothetical pathomechanisms. ...
Introduction
This study aimed to emphasize the importance of cranial nerve (CN) palsies in spontaneous cervical artery dissection (sCeAD).
Methods
A search term-based literature review was conducted on “cervical artery dissection” and “cranial nerve palsy.” English and German articles published until October 2023 were considered.
Results
Cranial nerve (CN) palsy in sCeAD is evident in approximately 10% of cases. In the literature, isolated palsies of CN II, III, VII, IX, X, and XII have been reported, while CN XI palsy only occurs in combination with other lower cranial nerve palsies. Dissection type and mural hematoma localization are specific to affected CN as CN palsies of II or III are solely evident in those with steno-occlusive vessel pathologies located at more proximal segments of ICA, while those with CN palsies of IX, X, XI, and XII occur in expansive sCeAD at more distal segments. This dichotomization emphasizes the hypothesis of a different pathomechanism in CN palsy associated with sCeAD, one being hypoperfusion or microembolism (CN II, III, and VII) and the other being a local mass effect on surrounding tissue (CN IX, X, XI, and XII). Clinically, the distinction between peripheral palsies and those caused by brainstem infarction is difficult. This differentiation is key, as, according to the reviewed cases, peripheral cranial nerve palsies in sCeAD patients mostly resolve completely over time, while those due to brainstem stroke do not, making cerebrovascular imaging appraisal essential.
Discussion
It is important to consider dissections as a potential cause of peripheral CN palsies and to be aware of the appropriate diagnostic pathways. This awareness can help clinicians make an early diagnosis, offering the opportunity for primary stroke prevention.
... Internal carotid artery dissection represented the most common specific cause overall, and the most frequent within the vascular etiology group. Carotid dissection occasionally presents with paresis of the cranial nerves and, to a greater extent, with lower cranial nerve compromise, with the XII CN being the most affected one [36,38,67,68,120]. In the literature, we found two hypotheses to explain the pathophysiology of lower CN palsy secondary to internal carotid dissection. ...
Collet-Sicard syndrome (CSS) is the unilateral palsy of the cranial nerves (CN) IX, X, XI, and XII. To our knowledge, no review describes the characteristics of patients diagnosed with CSS. Therefore, this review aims to collect and describe all cases in the literature labeled as CSS. We performed a scoping review of the literature and conducted a database search in Embase and PubMed. We included articles and abstracts with case reports or case series of patients with CSS diagnosis. We classified the cases into two groups: “CSS”, referring to patients presenting exclusively with IX-XII nerve involvement, and “CSS-plus”, which corresponds to cases with CSS and other neurological impairments. We included 135 patients from 126 articles, of which 84 (67.7%) were male. The most common clinical manifestations reported were dysphagia and dysphonia. The most common etiology was tumoral in 53 cases (39.6%) and vascular in 37 cases (27.6%). The majority of patients showed partial or total improvement, with just over half receiving conservative treatment. The most frequent anatomic space was the jugular foramen (44.4%) and the parapharyngeal retrostyloid space (28.9%). Approximately 21% of the patients had other CN impairments, with the seventh and eighth CN most frequently compromised. We conclude that although there is a need for greater rigor in CSS reporting, the syndrome has a clear utility in identifying the localization of jugular foramen and parapharyngeal retrostyloid space pathology.
... Symptoms of damage to the lower cranial nerves as a local symptom of dissection of the carotid artery are observed in 5-12% of patients with ICAD. In about 5.2% of cases, the damage to the lower cranial nerves (XII nerve, i.e., hypoglossal and additionally nerves IX, X, and XI in various combinations) is observed [3,[30][31][32][33][34]. Internal carotid artery dissection is one of the possible causes of damage to the mentioned cranial nerves [35]. ...
The diagnosis of internal carotid artery dissection (ICAD) at the stage of local signs is essential in the prevention of the life-treating cerebral complication; however, making this diagnosis has significant difficulties. We present the case of a 36-year-old female with left ICAD with asymmetric left-sided tongue swelling as an unusual and still unexpected symptom. The patient’s complaints at admission were left-sided numbness of the tongue and swallowing difficulties but its movements were intact. Despite the provided treatment for suspected angioedema, no improvement was noted. Additional examination revealed left-sided tongue weakness, ipsilateral soft palate palsy, paralysis and reduced tension of the left vocal fold, and left-sided Horner’s syndrome. Another suspected diagnosis was a dysfunction of the IX, X, and XII cranial nerves. A head MRI revealed an intramural hematoma of the left internal carotid artery. The radiologists suggested ICAD. The angio-MRI of the head arteries confirmed this diagnosis. The patient received dual antiplatelet therapy. The neuro-logopaedic therapy was also implemented. Currently, the patient’s symptoms are gradually improving with significantly better results on follow-up neuroimaging. Among the possible local symptoms of ICAD, proper attention should be paid to asymmetric swelling of the tongue as an atypical manifestation of damage to the hypoglossal nerve.
... To the best of our knowledge, a total of 37 cases of ICAD presenting with the lower cranial nerve palsy have been reported until 2018 [ Table 1]. [1][2][3][4][5][7][8][9][10][11][12][13][14][15]17,18,[20][21][22][23][24][25][26][27][28][29][30][31]33] Of the 37 cases, 34 were male. e side of dissection was left (n = 23), right (n = 11), or both (n = 3). ...
... No Anticoagulant N/A N/A Ishildak [14] 40/M Bilateral Ⅸ Ⅹ Ⅻ No No No Anticoagulant N/A N/A Nguyen et al. [26] 35/M Left Ⅹ N/A No No Antiplatelet Improve Recovery within 3 w Zeleňák et al. [33] 46/M Left Ⅸ Ⅹ Ⅺ Ⅻ Majeed et al. [18] 55/M Right ⅦiⅩ Ⅻ No No Yes Anticoagulant Improve Recovery of Ⅹ and Ⅻ palsy within 6 w: partial Horner's syndrome and y within 6 w: parti Hanyu [10] 40/M Right Ⅻ N/A No No N/A N/A N/A Heckmann et al. [12] 44/F Left Ⅸ Ⅹ Ⅺ Ⅻ Temporal, jaw ...
Background:
Some studies reported cases of internal carotid artery (ICA) dissection (ICAD) that was treated by carotid artery stenting (CAS). Symptoms of ICAD resulting from the lower cranial nerve palsy are rare and the treatment strategy is not clearly defined. We report a patient with ICAD showing hypoglossal nerve palsy alone that was treated by CAS.
Case description:
A 47-year-old man presented with headache, dysphagia, dysarthria, and tongue deviation to the left. He had no history of trauma nor any other significant medical history. Axial T2-CUBE MRI and MRA showed dissection of the left ICA accompanied with a false lumen. These findings indicated that direct compression by the false lumen was the cause of hypoglossal nerve palsy. Although medical treatment was continued, symptoms were not improved. Therefore, CAS was performed to thrombose the false lumen and decompress the hypoglossal nerve. His symptoms gradually improved after CAS and angiography performed at month 6 showed well-dilated ICA and disappearance of false lumen.
Conclusion:
CAS may be an effective treatment for the lower cranial nerve palsy caused by compression by a false lumen of ICAD.
... Patients with SLE and other connective tissue diseases have a higher risk of vascular dissection than the general population (8). Multiple factors are involved in the activation of autoimmune inflammation of the arterial walls such as immune complex formation and deposition, intimal damage, and medial extracellular matrix damage (9). According to a case report and literature review of 11 patients who presented with ischemic stroke as the initial manifestation of SLE, most patients (7/11), had ischemic infarcts in the vertebrobasilar artery and the pons was the most frequently affected region. ...
Brainstem infarction due to vertebrobasilar insufficiency is a rare initial presentation of systemic
lupus erythematosus (SLE) patients and small-vessel dissection as the direct cause of infarction
has not been reported. We report the case of a 20-year-old female with acute infarction on
the right side of the pons due to a small artery (pontine perforator) dissection, identified on
digital subtraction angiography and high-resolution vessel wall MRI (vwMRI). She was diagnosed
with SLE based on the presence of neurologic disorders and relevant laboratory findings.
The pontine perforator-dissecting aneurysm had occluded and the right distal vertebral
artery had resolved on subsequent vwMRI. She had a modified Rankin Scale (mRS) score of 1 at
discharge with mild symptom improvement, and exhibited no further aggravation of symptoms
at 3 or 12 months, maintaining an mRS score of 1.
... 7 Other symptoms include ipsilateral neck, facial or eye pain, ptosis, and visual disturbance. 1,3,8 Approximately 3-16% of patients with ICA dissection present with lower cranial nerve palsies. The most affected cranial nerves are X, XI, and XII. ...
... The most affected cranial nerves are X, XI, and XII. 3,8,9 As they exit the skull base through the jugular foramen and hypoglossal canal, these nerves travel in the carotid sheath and are therefore in close relation to the ICA, especially cranial nerves X and XII, which travel a longer distance along its length. In the neck, the vagus nerve can be found on both sides, and enters the carotid sheath and travels inferiorly between the common carotid artery and the internal jugular vein all the way to the base of the neck. ...
Internal carotid artery (ICA) dissection is a rare cause of a cranial nerve X palsy. Patients more commonly present with stroke or transient ischaemic attacks. An undetected and untreated ICA dissection can have serious consequences. Here, the authors present two cases of ICA dissection presenting with isolated vagal nerve palsy presenting with hoarseness. CT scans provided good evidence of ICA in both cases. The patients were treated with antiplatelet agents and made a good recovery with complete resolution of symptoms.
... or cervical pain accompany an acute HS, ICAD needs to be ruled out urgently. [3] In addition to causing HS by injuring the adjacent sympathetic plexus, an ICAD can compress local cranial nerves via pseudo-aneurysm 8-16% of the time, particularly IX-XII [4] and infrequently V and VII. [5] Cavernous sinus thrombosis also causes a 3 rd order HS but with ophthalmoparesis, particularly cranial nerve VI with no other brainstem signs. ...
A 57-year-old female presented with headache, miosis, and ptosis diagnosed as Horner syndrome (HS). After delaying the recommended diagnostic imaging, she experienced transient, unilateral visual impairment in bright light. The patient was subsequently determined to have a spontaneous internal carotid artery dissection (ICAD) and secondary retinal ischemia with minimal cardiovascular risk factors and no history of preceding trauma. She wore dark glasses, received gabapentin for pain control, and was anticoagulated for a total of 4 months at which time the ICAD resolved despite a residual blepharoptosis and anisocoria.
... Facial anhidrosis is usually not present because the facial sweat glands are innervated by the sympathetic plexus surrounding the external carotid artery (1,2). In 8-16% of cases there are symptoms of cranial nerve involvement, mostly concerning the lower cranial nerves (IX-XII) (8). An explanation for cranial nerve palsies is compression or stretching of the nerve by the expanded artery. ...
Background:
Carotid artery dissection (CAD) is a significant cause of ischemic stroke. Early recognition and treatment of CAD is important to prevent accompanying cerebral ischemia. This case report presents an atypical clinical presentation of CAD and emphasizes the diagnostic challenge for emergency physicians.
Case report:
A 54-year-old woman presented to the emergency department with a bilateral headache of 4 days' duration, hypesthesia of the left fifth cranial nerve, dysgeusia, and partial Horner syndrome on the left side. Magnetic resonance angiography showed a left-sided CAD without any signs of cerebral ischemic events. Antiplatelet therapy with clopidogrel was started, and the patient did not show any deterioration in the weeks thereafter. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: CAD can present with different combinations of cranial nerve palsies and should be in the differential diagnosis of dysgeusia and hypesthesia of the trigeminal nerve. Early recognition of CAD can be challenging in patients with rare cranial nerve involvement, but early treatment is crucial to prevent cerebral ischemic events.
... Arterial dissection is considered a very rare cause of ischaemic stroke; indeed, it has been reported that internal carotid artery dissection is responsible for <2% of all ischaemic strokes. 47,48 Similar to other connective tissue diseases, SLE has a higher risk of vascular dissection. The pathophysiological correlation between SLE and arterial dissection is not clearly known. ...
Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease that involves collagen tissue throughout the body. Several previous studies have shown that the risk of ischaemic and haemorrhagic stroke is significantly higher in SLE when compared to the general population, particularly in young individuals, representing one of the principal causes of death in these patients. Though the precise pathophysiology behind this increased risk is still poorly understood, several mechanisms are suggested to play a role. The high burden of cerebral small vessel disease features noted on brain neuroimaging studies, as well as the accelerated process of atherosclerosis identified in these patients, are likely to be responsible for at least some of the ischaemic strokes occurring in the SLE population. Repeated episodes of arterial and venous thrombosis secondary to antiphospholipid syndrome are likewise important. Less is known regarding the exact pathophysiological relationship between SLE and the high incidence of haemorrhagic stroke, though thrombocytopenia and a greater susceptibility to form typical and atypical brain aneurysms, which may then rupture, are thought to be the main mechanisms responsible for the occurrence of intracerebral and subarachnoid haemorrhage, respectively. Both inflammatory and noninflammatory events, all involving the immune system, are responsible for several pathological changes affecting cerebral vessels of every calibre in SLE, as confirmed by histopathology. In this context, endothelial activation and dysfunction play a critical role. This review will briefly analyse the most important factors responsible for the higher ischaemic and haemorrhagic stroke risk in the SLE population, with a particular focus on brain vascular changes.
... Moreover, stroke is the cause of 10%-15% of deaths in patients with SLE [5]. Internal carotid dissection (ICA) is considered a rare cause of ischemic stroke, accounting 2% of all ischemic events, and occurs most frequently in the fifth decade of life [6,7]. ...
... Horner's syndrome is seen in 28%-58% of cases of ICA dissections. Cranial nerves are involved in 8%-16% of cases, with lower cranial nerves IX-XII most commonly affected [6,7,14,15]. ...
Systemic lupus erythematosus (SLE) increases the risk of cerebrovascular events due to vascular changes, resulting in the weakening of the vessel walls. Moreover, patients with SLE have more incidence of arterial lesions such as dissections. Internal carotid dissection (ICA) is an infrequent cause of ischemic stroke, representing 2% of all ischemic events. We present a case of ischemic stroke, caused by a spontaneous dissection of intracranial ICA, treated with endovascular stent implantation, in a 22-year-old woman affected by SLE, newly diagnosed. ICA dissection with consequent ischemic stroke is an unusual first presentation of SLE disease. Our case highlights how, despite an infrequent occurrence, ICA dissection should be considered for young adults presenting with ischemic stroke, especially in those affected by SLE. This paper also shows the good technical result in the use of stenting in case of intracranial ICA dissection.
