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Some research suggests that mental health problems can be brought on by the stress of having unexplained symptom. In non-western cultures especially, psychological distress is often communicated through multiple somatic complaints. The biopsychosocial model takes into consideration all factors affecting health and disease, supporting the integration of biological, psychological and social factors in the assessment and treatment.
Objectives
In our study we assess prevalence of alexithymia as a potential psychopathological attribute manifesting as unexplained somatic symptoms
Methods
196 patients aged 18 to 60 with unexplained physical symptoms for at least three months, after collection of demographic data, medical and psychiatric history, were subject to Arabic version of the following scales : patient health questionnaire PHQ-15 to assess severity of somatic symptoms, patient health questionnaire PHQ-9 to assess depressive symptoms, generalized anaxiety disorder GAD-7 to assess general anxiety disorder symptoms and Toronto Alexithymia scale TAS to assess alexithymia
Results
90% of ours ample were female patients, 49,5% showed alexithymia, 27,6% were borderline alexithymic and 23% had no alexithymia. Patients with unexplained physical symptoms showed moderate to high depressive symptoms in 81,1% of the sample, moderate to severe anxiety symptoms in 73,5%. Severity of somatic symptoms as assessed by PHQ-15 were significantly highly correlated to scores for Alexithymia (TAS), depressive symptoms (PHQ-9) and anxiety symptoms (GAD-7) p<0,001
Conclusions
Alexithymia is prevalent among patients with unexplained physical symptoms. This later population has high prevalence of depressive and anxiety symptoms that go with the severity of somatic manifestations
Schizophrenia is associated with deficits in higher order processing of visual information, steady state visual evoked potential responses recorded over the occipital cortex in patients with schizophrenia suggest a dysfunction of lower level visual pathways, which was more prominent for magnocellular than parvocellular biased stimuli. The magnocellular pathway helps in orienting towards salient stimuli [1]. A magnocellular pathwad deficit could contribute to higher level visual cognitive deficits in schizophrenia dysfunction of the magnocellular pathway may also account for other well described aspects of neurophysiological dysfunction in schizophrenia, for example, the magnocellular pathway projects predominantly to dorsal cortical stream (i.e. parietal lobe), which codes motion perception and spatial localization [2].
Material
30 schizophrenic patients were recruited randomly from Alexandria University Hosiptal. They scored 4 or higher on the Clinical Global Impression Scale for Severity CGI-S. Visual Evoked Potential VEP was done to them and compared to healthy control group.
Results
In the right eye the mean P100 was 104.55 ± 5.62 and 95 ± 5.27 msec in schizophrenic and healthy control group respectively with statistical significant difference. A finding that has been replicated in the left eye where the mean P100 was 105.8 ± 5.41 and 95.85 ± 5.4 msec in the same respective groups
Conclusion
P100 in both right and left eyes are more prolonged in schizophrenic patients compared to healthy control groups.
Transient neurological symptoms often present a difficult diagnostic dilemma. It is often difficult to tell if the transient symptoms were due to ischemia or due to something else (see Chapter 1). Usually, by the time the physician sees the patient, the neurological exam has returned to normal. On the other hand, it is critically important not to miss the diagnosis of transient ischemic attack (TIA). TIAs may provide an opportunity for physicians to intervene and prevent an ischemic stroke and subsequent disability, and must be taken seriously. The search for an etiology must be done expeditiously. Just as angina may serve as a warning for future myocardial infarction, a TIA is often a warning sign of an impending stroke.
As acute stroke therapies have developed, the context in which stroke care is provided has become more important. Creating and maintaining the organization of stroke care within a region or even a hospital requires much commitment and effort. High-quality stroke care requires coordination and communication between multiple stakeholders in the prehospital and in-hospital settings in what the American Heart Association (AHA) and American Stroke Association (ASA) term the “stroke chain of survival” (Table 14.1).
It is never too early to begin to educate the patient and family about lifestyle changes and medical treatments to prevent another stroke. These need to be reinforced throughout the hospital and rehabilitation stay, and in the outpatient stroke clinic.
After a major stroke, both the family and the patient go through a grief reaction that at first includes denial and disbelief, and sometimes anger. In particular, the need to insert a PEG is often a crisis point when the family finally comes to terms with the severe disability and prolonged recovery that lies ahead. At this stage, which is usually when the patient is in the acute stroke unit, mainly supportive measures are indicated.
In this chapter, we discuss mainly secondary prevention for stroke, although many of the measures, especially control of risk factors and lifestyle changes such as not smoking, controlling blood pressure, etc., are also important measures to avoid a first stroke.
Initially, we discuss a tailored diagnostic work-up, then general measures for secondary prevention of ischemic stroke, and finally recommendations for specific conditions that are associated with a high risk of recurrent stroke.
The following initial measures apply to all stroke patients. They are necessary to stabilize and assess the patient, and prepare for definitive therapy. All current and, probably, future stroke therapies for both ischemic and hemorrhagic stroke are best implemented as fast as possible, so these things need to be done quickly. This is the general order to do things, but in reality, in order to speed the process, these measures are usually dealt with simultaneously. They are best addressed in the ED, where urgent care pathways for stroke should be established and part of the routine (see Chapter 14).
This chapter covers the diagnosis and management of spontaneous subarachnoid hemorrhage due to rupture of intracranial aneurysms. At the end of the chapter we also discuss unruptured intracranial aneurysms. Much SAH management is not based on good-quality evidence. Much of what is recommended here comes from published practice guidelines and what is commonly practiced. Options for therapy might be limited by the availability and experience of persons performing surgery, endovascular therapy, and neurointensive care.
In this chapter, we consider spontaneous hemorrhage into the brain parenchyma and ventricles (intracerebral hemorrhage, ICH). Non-traumatic bleeding into the subarachnoid space (subarachnoid hemorrhage, SAH) is covered in Chapter 13. Traumatic subdural and epidural hemorrhages are not covered in this book.
Intracerebral hemorrhage is associated with very high morbidity and mortality. It is important to realize that, as with acute ischemic strokes, time is of the essence in ICH. The reason for this is that the blood accumulates rapidly, and the volume of the hematoma is the most important determinant of outcome.
Cerebral venous sinus thrombosis (CVST) is the thrombosis of dural venous sinuses and/or cerebral veins. It accounts for 0.5% of all strokes. It occurs predominantly in the younger population (usually < 50 years old, median age of 37). Female-to-male ratio is 3 to 1, likely secondary to sex-specific thrombogenic states including pregnancy, puerperium, oral contraceptive pill use, and hormonal therapy.
When used alone, intravenous and intra-arterial thrombolysis have yielded low recanalization rates of proximal large-vessel occlusions (LVO). The endovascular trials utilizing first-generation devices such as the Merci retriever and the Penumbra aspiration system were essentially neutral and failed to demonstrate superiority of mechanical thrombectomy over IV tPA (MR RESCUE, SYNTHESIS, IMS-III). In 2015, however, six trials – MR CLEAN, EXTEND-IA, SWIFT PRIME, ESCAPE, REVASCAT, and THRACE – led to a fundamental shift in how we acutely manage LVOs today. All six trials compared endovascular thrombectomy (EVT) to IV tPA alone and demonstrated clear superiority of thrombectomy in patients presenting within 6 hours from the time they were last known well (LKW) if they met specific imaging criteria.
This chapter discusses the four main components of acute ischemic stroke care. The sections on prevention of complications, and recovery and rehabilitation, are applicable to both ischemic and hemorrhagic stroke patients.
Although, classically, stroke symptoms are maximal at onset and patients gradually recover over days, weeks, and months, patients sometimes deteriorate. People have termed the phenomenon stroke progression, stroke in evolution, stroke deterioration, and symptom fluctuation. There is no consistent terminology. The phenomenon occurs from different causes and is incompletely understood. Although the typical definition of a significant neurological deterioration in trials has been a gain of ≥ 1 point on item 1a (level of consciousness) or ≥ 4 points in the motor items of the NIHSS, any detectable deterioration should prompt careful assessment and a tailored work-up.