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Ann Indian Acad Neurol
Ann Indian Acad Neurol
AIAN
Ann Indian Acad Neurol
Annals of Indian Academy of Neurology
0972-2327
1998-3549
Wolters Kluwer - Medknow India

AIAN-27-457
10.4103/aian.aian_134_24
Letters to the Editor
Cervical Artery Dissection: Clinical Outcomes and Functional Outcome Predictors from a Tertiary Care Center in India
Agarwal Ayush
Garg Ajay 1
Antil Yamini
Bhatia Rohit
Joseph Leve 1
Sharma Agrata
Agarwal Sushant 1
Upadhyay Ashish 2
Vishnu Venugopalan Y.
Srivastava M. V. Padma
Department of Neurology, All India Institute of Medical Sciences, New Delhi, India
1 Department of Neuroimaging and Interventional Neuroradiology, All India Institute of Medical Sciences, New Delhi, India
2 Department of Biostatistics, All India Institute of Medical Sciences, New Delhi, India
Address for correspondence: Prof. M. V. Padma Srivastava, Head of Department of Neurology, Chief, Neurosciences Centre, AIIMS, New Delhi, India. E-mail: Vasanthapadma123@gmail.com
Jul-Aug 2024
18 7 2024
27 4 457460
22 2 2024
18 4 2024
25 4 2024
Copyright: © 2024 Annals of Indian Academy of Neurology
2024
https://creativecommons.org/licenses/by-nc-sa/4.0/ This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.
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pmcDear Editor,

Cervical artery dissection (CAD) is defined as the collection of blood in between the arterial wall layers of either the internal carotid or vertebral arteries. It results from an intimal tear in the arterial wall, leading to a false lumen formation allowing blood to enter and form a mural hematoma. The exact pathophysiology of CAD is unclear. It is considered to be a multifactorial disease, with environmental factors acting as potential triggers in genetically predisposed individuals.[1] It can occur either spontaneously or secondary to traumatic injury. Although the overall incidence of CAD is 2.6–3 per 100,000 people per year,[1] it accounts for 15%–24% cases of stroke in young people.[23] CAD involving the internal carotid artery (ICA) is commoner than that involving the vertebral artery. The symptoms resulting from dissection result either from ischemia secondary to intraluminal stenosis/occlusion or from compression by intramural hematoma of the adjacent nerves.[45] Neuroimaging is used to confirm CAD diagnosis, and classical findings on vascular imaging include the crescent sign, tapered arterial stenosis/occlusion, presence of a vascular flap or double lumen, and a dissecting aneurysm.[1] Management involves the use of antithrombotic therapy in the form of either antiplatelets or anticoagulants.[6] The recurrence risk is low, especially occurring in a few weeks poststroke. Only a few studies from India have looked at the demographic, imaging, and outcome features of CAD due to its comparative rarity. Our study was conducted to delineate these features and find differences in risk factors, imaging, or outcome profiles when compared to other described cohorts.

We retrospectively analyzed data from our cohort of acute ischemic stroke patients who presented to a tertiary care center between December 2016 and December 2022. All stroke patients ≥18 years old were screened for their stroke etiology, and patients with CAD were recruited. Data of all included patients was entered into a previously drafted proforma by two neurologists. All imaging data was verified and entered by a neuroradiologist. Parenchymal imaging was conducted using a non-contrast computed tomography of the head or magnetic resonance imaging of the brain. Vascular imaging was conducted using a computed tomography angiogram. The imaging criteria used to diagnose CAD were the presence of a narrow or eccentric lumen surrounded by a crescent-shaped mural thickening, an abrupt or tapered lumen, presence of aneurysms with luminal narrowing, or the presence of a luminal flap. Recanalization status was assessed via repeat vascular imaging between 3 and 6 months post-index event, and patients were dichotomized into recanalized (complete recanalization) and non-recanalized (partial or no recanalization). A good functional outcome was described as a modified Rankin Score (mRS) ≤2. Treatment with either antiplatelets or anticoagulants was at the discretion of the treating neurologist. The patients were followed up for a minimum duration of 6 months and up to 5 years. Anyone who was smoking or consuming alcohol actively before stroke occurrence was considered to have a presence of these risk factors. The main outcomes assessed were factors determining functional independence (mRS: 0–2) at the last follow-up and differences in outcome between patients with and without recanalization.

Statistical analysis was conducted using STATA version 17.0. Continuous variables were expressed as median with interquartile range, and categorical variables as numbers with respective percentages. Pearson’s Chi-square test and Wilcoxon rank-sum test were used as appropriate.

We recruited 65 CAD patients with a median age of 38 years and a male predominance (5.5:1). Hemiparesis was the most common presentation (76%). The median Alberta Stroke Programme Early Computed Tomography Score (ASPECTS) and National Institute of Health Stroke Scale (NIHSS) scores at admission were 8 and 9, respectively. Only three of our patients presented within the window period (≤4.5 h) and were thrombolysed with alteplase. No patient underwent endovascular thrombectomy. The average duration of hospital stay was 7 days with a median mRS at discharge of 3. Fifty-three of our patients (81.5%) were treated with antiplatelets (18- single and 35- dual antiplatelets), while the rest received anticoagulation (1- warfarin, 11- acitrom; no patient received direct oral anticoagulants). The median mRS at the last follow-up was 1, mRS between 0 and 2 was achieved in 46/65 (70.1%) patients, and eight patients (12.3%) died [Figure 1]. There were no stroke recurrences. Patients who received anticoagulation were switched to antiplatelets after 6 months of treatment, irrespective of the recanalization status, and patients receiving antiplatelets were continued on the same. The clinical and radiologic findings of our patients are presented in Table 1 and Supplementary Table 1, respectively.

Figure 1 mRS distribution at discharge and last follow up. mRS = modified Rankin Score

Table 1 Patient characteristics

	n=65	
Median age at presentation in years (IQR)	38 (30-48)	
Gender (M:F)	55:10	
Median symptom duration to admission in days (IQR)	7(5-2)	
Median NIHSS at admission (IQR)	9(6-13)	
Presenting symptoms, n (%)	
    • Hemiparesis	50 (76.9)	
    • Vertigo士dysarthria	13 (20)	
    • Ataxia	5 (7.7)	
    • Diplopia	1 (1.55)	
    • Neck pain	22 (33.8)	
    • Vision loss	4 (6.2)	
    • Seizures	9(13.8)	
Median mRS at discharge (IQR)	3 (2-4)	
Median duration of follow-up	33 months	
Median mRS at the last follow-up (IQR)	1 (0-3)	
Median ASPECTS score (IQR)	8 (6-9)	
mRS distribution at the last follow-up	
    0	17	
    1	21	
    2	8	
    3	8	
    4	3	
    5	0	
    6	8	
F=Female, IQR=Interquartile range, M=Male, mRS=Modified Rankin Score

Supplementary Table 1 Radiological findings

	n=65	
Vessel involved n (%)	
    Internal carotid artery	43 (66.2)	
    Vertebral artery	22 (33.8)	
Side involved n (%)	
    Right	32 (49.2)	
    Left	32 (49.2)	
    Both	1(1.6)	
Site of involvement n (%)	
    Extracranial ICA	33 (50.8)	
    Intracranial ICA	10(15.4)	
    V1 segment	18 (27.7)	
    V3-V4 segment	4(6.1)	
Presence of luminal flap n (%)	21 (32.3)	
Type of infarct n (%)	
    Embolic	46 (70.7)	
    Watershed	19 (29.3)	
    Presence of filling defect n (%)	51 (78.5)	
Type of occlusion n (%)	
    Tapered	58 (89.2)	
    Abrupt	7(10.8)	
Lumen type n (%)	
    Narrow	25 (38.5)	
    Eccentric	40(61.5)	
Occlusion n (%)	
    Partial	22 (33.8)	
    Complete	43 (66.2)	
Recanalization status (n=32) n (%)	
    Complete recanalization	10(31.2)	
    Non-recanlized (Partial or none)	22 (68.8)	
ICA=internal carotid artery

Patients who achieved a good functional outcome had a lower NIHSS score at admission and lower mRS score at discharge (P = 0.001 for both), lower prevalence of diabetes (P = 0.009) and smoking (P = 0.045), and higher hemoglobin levels at admission (P = 0.001) [Table 2].

Table 2 Good versus poor functional outcome

	mRS 0-2 (n=46)	mRS 3-6 (n=19)	P	
Median age (in years)	38 (30-48)	38 (32-50)	0.825	
Gender (male:female)	39:7	16:3	0.954	
Median hospital stay duration (in days)	6(4.5-11)	8(5-15)	0.240	
Median NIHSS at admission	8(6-10)	12 (6-13)	0.001	
Median mRS at discharge	2(1-4)	4(3-5)	0.001	
Median SBP in mmHg	132 (120-140)	130 (123-140)	0.375	
Median DBP in mmHg	80 (74-90)	80 (78-82)	0.558	
Median pulse in per min	76 (70-86)	85 (78-88)	0.964	
Stroke territory			0.773	
    Anterior	30 (65.2)	13 (68.4)		
    Posterior	16 (34.8)	6(31.6)		
Wake-up stroke			0.985	
    Yes	12(26.1)	5 (26.3)		
    No	34(73.9)	14(73.7)		
Symptoms, n (%)				
    • Hemiparesis	35 (76.1)	15 (78.9)	0.803	
    • Vertigo士dysarthria	11 (23.9)	2 (10.5)	0.220	
    • Ataxia	3 (6.5)	2 (10.5)	0.582	
    • Diplopia	0	1 (5.2)	0.117	
    • Neck pain	18 (39.1)	4(21)	0.161	
    • Vision loss	2 (4.3)	2 (10.5)	0.346	
    • Seizures	7(15.2)	2(10.5)	0.618	
Risk factors, n (%)	
    • Diabetes	2 (4.3)	5 (26.3)	0.009	
    • Hypertension	14 (30.4)	5 (26.3)	0.740	
    • Dyslipidemia	0	0		
    • Coronary artery disease	2 (4.3)	1 (5.2)	0.873	
    • Atrial fibrillation	0	1 (5.2)	0.117	
    • Smoking	22 (47.8)	4(21)	0.045	
    • Alcohol	9(19.6)	3 (15.8)	0.721	
    • Recreational drug use	0	0		
    • Fever	1 (2.1)	0	0.517	
    • Migraine	2 (4.3)	0	0.356	
    • Prior TIA	4 (8.7)	3 (15.8)	0.401	
    • Prior stroke	4 (8.7)	2 (10.5)	0.817	
    • Family h/o stroke	3 (6.5)	1 (5.2)	0.848	
Site of dissection, n (%)			0.738	
    • ICA	29(63.1)	14(73.6)		
    • VA	17 (36.9)	5 (26.4)		
Laterality, n (%)			0.781	
    • Right	22 (47.8)	10 (52.6)		
    • Left	23 (50)	9 (47.4)		
    • Both	1 (2.2)	0		
Imaging findings, n (%)			0.834	
    • Embolic	32 (69.5)	14 (73.8)		
    • Watershed	14 (30.5)	5 (26.2)		
Treatment, n (%)				
    • Antiplatelets	37 (80.4)	15 (78.9)	0.721	
    • Anticoagulation	9(19.6)	4(21.1)	0.729	
Recanalized artery (n=10), n (%)	8(30.8)	2 (33.3)	0.903	
Investigations	
    • Hemoglobin	14.5 g/dl (13.2-15.8)	12.8 g/dl (11-15.2)	0.001	
    • TLC in ×103 per mm3	9 (7.2-10.1)	8.5 (6.6-11.6)	0.395	
    • Platelet count in x103 per mm3	229.5 (163-292)	242 (181-317)	0.622	
    • ESR	12 (6-18)	13 (8-16)	0.492	
    • CRP 2.7 (1.2-14.1)	6.2 (1.5-35.5)	0.284		
    • S. creatinine 0.8 mg/dl (0.6-0.9)	0.7 mg/dl (0.6-0.8)	0.070		
    • HbA1c 5.5% (5.2-5.8)	5.7% (5.2-9.8)	0.991		
    • Homocysteine 19 (11.4-42.2)	17.4 (12.9-35.6)	0.949		
    • Triglycerides 134 (91-152)	137.5 (81-186)	0.780		
    • LDL 85.5 (67-126)	93.1 (75-112)	0.847		
    • HDL 38 (32-44)	34.5 (29-42)	0.084		
CRP=C-reactive protein, DBP=diastolic blood pressure, ESR=erythrocyte sedimentation rate, HbA1c=hemoglobin A1c, HDL=high-density lipoprotein, ICA=internal carotid artery, LDL=low-density lipoprotein, mRS=modified Rankin Score, SBP=systolic blood pressure, TIA=transient ischemic attack, TLC=total leukocyte count, VA=vertebral artery. All continuous variables are expressed as Median (IQR) and the categorical variables are expressed as frequency and percentage

Majority of the patients presented with ICA dissection, embolic infarcts (70.7%) were commoner, and complete occlusion occurred in 66.7% patients. Complete recanalization was seen in 31.2%. There was no difference in functional outcome between patients based on recanalization status [Supplementary Table 2].

Supplementary Table 2 Differences between patients with or without recanalization of dissected artery (n=32)

	Recanalized (n=10)	Not recanalized (n=22)	P	
Median Age in years	35 (27-40)	35.5 (30-45)	0.729	
Hospital stay in days (median)	9(4-12)	6(4-11)	0.775	
Treatment used			0.131	
    Antiplatelet	7 (70%)	20 (90.9%)		
    Anticoagulants	3 (30%)	2(9.1%)		
Dissection site			0.725	
    ICA	7 (70%)	14 (63.6%)		
    VA	3 (30%)	8 (36.4%)		
Infarct pattern			0.244	
    Embolic	5 (50%)	15 (71.4%)		
    Watershed	5 (50%)	7 (28.6%)		
Filling defect with thrombus present	6 (60%)	18(81.8%)	0.186	
Tapered occlusion (non-abrupt)	10 (100%)	20 (90.9%)	0.325	
Luminal findings			0.017	
    Narrow lumen	0	9 (40.9%)		
    Eccentric lumen	10 (100%)	13 (59.1%)		
Clinical features				
    Median NIHSS at discharge	5(4-12)	5.5 (3-10)	0.407	
    Median mRS at discharge	3 (2-4)	3 (2-4)	0.919	
    SBP in mm Hg	130 (126-136)	130 (116-152)	0.752	
    DBP in mm Hg	80 (74-80)	80 (73-90)	0.691	
Labortaory features				
    Hb in gm/dl	14.7(12.8-15.8)	14.5 (13-15.9)	0.477	
    TLC (×103/mm3)	9.8 (7.6-11.9)	9.5 (7.2-10.7)	0.212	
    Platelets (×103/mm3)	238 (172.4-256)	258 (155-304)	0.700	
    Creatinine	0.7mg/dl (0.6-0.8)	0.8mg/dl (0.6-1)	0.913	
    Homocysteine	12.5mg/dl (11.4-25.6)	22.5mg/dl (13.7-48.8)	0.247	
    B12	223 (190-388)	336 (221-572)	0.276	
    CRP	2.1 (1.2-8.7)	3.2 (1.5-25)	0.317	
    ESR in mm/hr	10(5-16)	11 (7-15)	0.771	
    HbAlc (%)	5.2 (4.9-5.4)	5.5 (5.2-5.6)	0.453	
    LDL	84 (65-107)	116 (72-136)	0.946	
    HDL	39 (38-44)	32.5 (28-43)	0.016	
ICA=Internal carotid artery, VA=Vertebral artery, NIHSS=National institute of health stroke scale, mRS=modified Rankin scale, SBP=Systolic blood pressure, DBP=Diastolic blood pressure, Hb=Hemoglobin, TLC=Total leukocyte count, CRP=C Reactive Protein, ESR=Erythrocyte sedimentation rate, HbA1c=Glycated haemoglobin, LDL=Low density lipoprotein, HDL=High density lipoprotein. All the continuous variables are expressed as median (IQR) and categorical variables are expressed frequency and percentage

The presence of diabetes (P = 0.009) and smoking (P = 0.045) was associated with poorer functional outcomes. Previous studies have proven diabetes to be associated with worse functional outcomes and stroke mortality.[7] Liang et al.,[8] in their study, analyzed 9087 young Taiwanese stroke patients and demonstrated smoking to be associated with a higher risk of unfavorable outcome at 3 months poststroke. Homocysteine levels were found to be elevated in 24 out of the 45 tested, with five patients having values >65 mg/dl. Hyperhomocysteinemia is a risk factor for CAD that leads to inherent vessel wall weakness, which dissects following minor superadded environmental factors.[9] Recanalization was assessed at 6 months in 32 patients in our cohort, and 10 patients were found to have completely recanalized. However, the outcome did not differ between patients with and without recanalization. Similar findings were reported by Wadhwa et al.[10]

CAD is an important cause of stroke in young people. The presence of severe stroke symptoms at presentation and discharge, diabetes mellitus, smoking, and lower hemoglobin levels were associated with worse outcomes. However, the recanalization status of the afflicted vessel did not affect the functional outcome post-CAD.

Institutional ethics clearance was taken from the institutional ethics committee (IEC-914/3.01.20).

Financial support and sponsorship

The study was supported by a grant from Department of Biotechnology, Government of India (BT/PR33179/AI/133/16/2019).

Conflicts of interest

There are no conflicts of interest.
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