Cerebrovascular accidents (CVA) is the third leading cause of death in the developed world, after heart diseases and cancer (Ojaghihaghighi et al, 2017). Approximately, 600,000 new cases each year and an estimated 4.5 million stroke survivors reside currently in the United States. The continued improvement of the management of acute stroke will increase the number of stroke survivors(Whyte & Mulsant, 2002).
In survivors, CVA is considered as the most common cause of morbidity and prominent disability. Stroke causes often major changes in a person’s life: stroke survivors may have loss of health, occupation, social role, and independence(Whyte ; Mulsant, 2002). Where in the few months after a CVA event 20% of patients will be in need of medical care and rehabilitation procedures. On the other hand, a significant proportion of health care is wasted on CVA (Ojaghihaghighi et al, 2017).
In brain, the rupture or occlusion of blood vessels results in stroke. At onset, the deficits resulting from stroke are usually maximal (in contrast to symptoms of a brain tumor that are steadily worsening), continue for more than 24 hours and coincide with injury to the brain’s vasculature as determined by neurological and neuroimaging examination. Muscle weakness, problems with vision, loss of sensation, and impaired speech are the typical symptoms of stroke. Additional symptoms, including loss of consciousness, may occur depending on the location and severity of neural damage.
The main types of stroke are two: hemorrhagic and thrombotic (known also as ischemic). 20% of CVA are hemorrhagic which can be caused by a ruptured cerebral blood vessel, a ruptured intracranial aneurysm or an arterio-venous malformation leading to an intracerebral hemorrhage in or near the brain. The 2 different subtypes of hemorrhagic stroke are intracerebral hemorrhage (ICH)manifested by direct bleeding into the brain parenchyma and, subarachnoid hemorrhage(SAH)manifested by bleeding into the cerebrospinal fluid (CSF)(Smith & Eskey, 2011). A thrombotic stroke account for 80% of CVA. The occlusion of one or more cerebral blood vessel results in thrombotic stroke. Directly, a thrombus can form on a diseased small vessel, or a large vessel atherosclerotic plaque can embolize and block a small cerebral artery. An ischemic stroke is subclassified as lacunar stroke, cardioembolic stroke, large artery stroke or unknown ischemic type(Chapman et al., 2004).
Lacunar stroke, also called subcortical infarcts, is caused by the obstruction of a single penetrating artery and constitute one quarter of cerebral infarctions. Classical lacunar syndrome (pure motor hemiparesis, sensory motor stroke, pure sensory syndrome, ataxic hemiparesis or dysarthria clumsy-hand) is usually seen in lacunar infarct patients. Major risk factor for lacunar stroke are hypertension and diabetes mellitus(Arboix & Martí-Vilalta, 2009). In other hand, cardioembolic stroke refers to arterial obstruction resulting from embolus arising in the heart. Large artery atherosclerosis consist in obstruction of a major artery resulting from atherosclerosis, impairment of cerebral cortex (aphasia, restricted motor involvement, neglect) or brain stem or cerebellar dysfunction are seen(Adams & Biller, 2015).
Unknown ischemic type is a stroke in which the cause cannot be identified with any degree of confidence. Patients may have two or more causes of stroke or no cause is detected so a final diagnosis cannot be generated by the physician(Adams & Biller, 2015).
Another presentation of stroke is the transient ischemic attack (TIA) which is a temporary interruption of the blood supply to a region of the brain. It results usually from narrowing of the carotid arteries due to a plaque accumulation (carotid stenosis). A sudden onset of stroke symptoms and a focal loss of brain function lasting less than 24 hours are experienced by TIA’s patients. According to World Health Organization criteria (WHO) TIA is thought to be due to arterioembolic or thrombotic vascular disease(Chapman et al., 2004). Between 8 and 33% of TIA’s patients go on to have full stroke within 2 to 5 years of their first TIA according to studies from United States and Europe.
Stroke survivors may have mood disorders which are common in post stroke patients and are associated with increased morbidity and mortality. One third of stroke survivors develop post stroke depression and one quarter develop post stroke anxiety according to meta-analyses of point prevalence rates(Broomfield, Quinn, Abdul-Rahim, Walters, & Evans, 2014).
The mismatch between the feeling and the expression lead to anxiety. People, for example, seem to be laughing when they actually feel concern, therefore these people are vulnerable to rapid mood change(Sianturi, Anna Keliat, & Yulia Wardani, 2018).
Anxiety disorder or anxiety caseness causes reduction of quality of life, increase in health utilization and disabling health conditions and may even increase risk of death(Campbell Burton et al., 2013).
Anxiety disorder is classified according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (6) classi?es anxiety disorders as a collection of individual syndromes that include generalized anxiety disorder (GAD), panic disorder (with or without agoraphobia), agoraphobia (with or without panic), speci?c phobia, social phobia, obsessive compulsive disorder (OCD), posttraumatic stress disorder (PTSD), acute stress disorder, anxiety disorder due to a general medical condition, substance induced anxiety disorder, and anxiety disorder not otherwise speci?ed(Campbell Burton et al., 2013).
An excessive and inappropriate worrying that is persistent and restricted to particular circumstances are the main characteristics of generalized anxiety disorder (GAD). Patients experience physical anxiety symptoms (such as tremor and tachycardia) and key psychological symptoms that include: fatigue, restlessness, irritability, difficulty in concentrating and disturbed sleep. GAD is disabling and common, 12 months prevalence of between 1.7 % and 3.75% (more common in old age) is reported by recent review of epidemiological studies in Europe(Carobrez, Kincheski, & Bertoglio, 2010).
Compared to stroke related physical disabilities, post stroke mood disorders are relatively underesearched despite their prevalence(Broomfield et al., 2014). These disorders were in the past seen by clinicians as understandable psychological reaction to disability with little need for therapeutic intervention. However, in the last decade a number of review articles indicated that there has been a rapid expansion in the amount of research concerning this aspect of the outcome of stroke. This unpleasant states of mode may be a part of the morbidity of stroke by impairing cognitive function, by impeding rehabilitation or by contributing to the stress on caregivers(Johnson et al., 1995).
Only recently, post stroke anxiety has gained attention. Most probably this is due to the low prevalence reported in early population based studies on PSA, which is consistent with epidemiological results from the general adult population, that have been suggested that among older adults anxiety is uncommon. Concerning the usability of depression and anxiety rating scales in neurologic patients, it has been obvious that these are rather sensitive to distress rather than specific for identifying depressive and anxiety disorders(Schöttke & Giabbiconi, 2015).
Some studies show a prevalence of 12±28% of post-stroke anxiety disorders(Sembi, Tarrier, O’Neill, Burns, ; Faragher, 1998) which may be more common than is generally recognized(Johnson et al., 1995). Among a group of 99 Australian patients seen examined 2 to 3 months after a stroke, a frequency of 3% for DSM? diagnosed generalized anxiety disorders is reported by Moris et al, also among 89 community- based stroke patients seen 1 month after cerebral infarct, a frequency of 3.5% for ICD-9 defined anxiety neurosis is reported by House et al(Castillo, Starkstein, Fedoroff, Price, ; Robinson, 1993), and among 98 acute stroke patients, a prevalence of 6% for modified DSM-III-defined generalized anxiety disorder is reported by Skartestein et al(Castillo, Schultz, ; Robinson, 1995).
Point prevalence of anxiety is markedly higher after stroke, compared to general population. This prevalence remains high up to 5 years after stroke as indicated by longitudinal studies(Liu, Cai, Zhang, Zhu, ; He, 2018). Few other studies showed that approximately one third of PSA patients had a history of mood or anxiety disorders(Schöttke ; Giabbiconi, 2015). In the first 5 years after stroke 24% of patients with stroke had anxiety symptoms and 18% had an anxiety disorder as reported by a systematic review including 39 cohorts and 4706 patients (Kim, J.S, 2016).
A study assessing emotional symptoms in acute ischemic stroke have shown a clinically significant anxiety symptoms in 25% of the patients with acute ischemic stroke(Fure, Wyller, Engedal, ; Thommessen, 2006). While, other study have been shown a poor long-term psychological consequences including anxiety and depression will be present in one in five of SAH survivors(Turi et al., 2018). Berry E. have shown that 18% of SAH patients will be found to have anxiety as main presenting problem and, Morris et al have been reported that a significant levels of anxiety is presented in approximately 40% of SAH survivors more than 16 months after SAH.(Morris, Wilson, ; Dunn, 2004).
Post stroke anxiety can due to physical disability as studies showed that physical impact of stroke leads to psychological impact, especially, during the first post-stroke stage, at which clients experience anxiety and low self-acceptance up to 28 days(Sianturi et al., 2018).
While one study reported that prevalence of post stroke anxiety decreased over time (at 3 month 33%, at 2 years 18%), another study showed no variations over 3 years after stroke. When it associated with post stroke depression (PSD), PSA tends to last longer (Kim,J.S,2016).
In term of injury characteristics, an association between persistent mood disorders and the site of stroke induced brain damage is reported by Robinson and co-workers from John Hopkins School of Medicine(Sharpe et al., 1990). A significant correlation is found between PSA and right hemisphere lesions, while a correlation with hemisphere lesions is found in co-morbid PSA and PSD. Castillo et al. identify a more prevalent association of anxiety with posterior right hemisphere lesions. The results of this study shows that anxiety and depression experienced 3 months after stroke and that lesions in the left hemisphere may be correlated to increased anxiety and depression scores(Barker-Collo, 2007). Hsiao et al. found at the end of the first month after stroke that lesions in the posterior part of the superior and middle temporal gyrus were correlated with higher anxiety. Other studies on animal presented an important role of temporal structures in anxiety(Ku et al., 2013).
Aim of the study:
Our aim is to study the correlation of anxiety with the different subtypes of cerebrovascu