A transient ischemic attack (spelled ischaemic in British English)[1] (abbreviated as TIA, often referred to as "mini stroke") is a transient episode

of neurologic dysfunction caused by ischemia (loss of blood flow) - either focal brain, spinal cord, or retinal - without acute infarction (tissue death). The symptoms of a TIA can resolve within a few minutes unlike a stroke. TIAs share the same underlying etiology (cause) as strokes; a disruption of cerebral blood flow (CBF). TIAs and strokes present with the same symptoms such as contralateral paralysis (opposite side of body from affected brain hemisphere), or sudden weakness or numbness. A TIA may cause sudden dimming or loss of vision, aphasia, slurred speech and mental confusion. The symptoms of a TIA typically resolve within 24 hours unlike a stroke. Brain injury may still occur in a TIA lasting only a few minutes. Having a TIA is a risk factor for eventually having a stroke or a silent stroke. [2][3]A silent stroke or silent cerebral infarct (SCI) differs from a TIA in that there are no immediately observable symptoms. A SCI may still cause long lasting neurological dysfunction affecting such areas as mood, personality and cognition. A SCI is often a precursor to having a TIA or major stroke as well as occurring after an initial TIA or major stroke.[4] A cerebral infarct that lasts longer than 24 hours but fewer than 72 hours is termed a reversible ischemic neurologic deficit or RIND.

Contents
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1 Symptoms 2 Diagnosis 3 Effects of a TIA o 3.1 Prognosis o 3.2 Causes 4 Alternative diagnoses 5 Prevention 6 Treatment o 6.1 Medication 7 Risk factors 8 References 9 External links

Symptoms
Symptoms vary widely from person to person, depending on the area of the brain involved. The most frequent symptoms include temporary loss of vision (typically amaurosis fugax); difficulty speaking (aphasia); weakness on one side of the body (hemiparesis); and numbness or tingling (paresthesia), usually on one side of the body. Impairment of consciousness is very uncommon. There have been cases of temporary and partial paralysis affecting the face and tongue of the afflicted. The symptoms of a TIA are short lived and usually last a few seconds to a few minutes

and most symptoms disappear within 60 minutes. Some individuals may have a lingering feeling that something odd happened to the body. Dizziness, lack of coordination or poor balance are also symptoms related to TIA. Symptoms will vary in severity.

Diagnosis
TIA will usually be diagnosed after a doctor performs a history and a physical exam. There are several radiological tests that are done to evaluate patients who have had a TIA. This includes a CT scan or an MRI of the brain, Ultrasound of the neck, an echocardiogram of the heart. In most cases, the source of atherosclerosis is usually identified with an ultrasound.[5]

Effects of a TIA
Prognosis
Patients diagnosed with a TIA are sometimes said to have had a warning for an approaching stroke. If the time period of blood supply impairment lasts more than a few minutes, the nerve cells of that area of the brain die and cause permanent neurologic deficit. One third of the people with TIA later have recurrent TIAs and one third have a stroke because of permanent nerve cell loss.[6][not in citation given]

Causes
The most common cause of a TIA is an embolus that occludes an artery in the brain. This most frequently arises from a dislodged atherosclerotic plaque in one of the carotid arteries (i.e. a number of major arteries in the head and neck) or from a thrombus (i.e. a blood clot) in the heart because of atrial fibrillation. In a TIA, the blockage period is very short lived and hence there is no permanent damage.[7] The cholesterol build-up is gradual and eventually narrows the lumen. With time, blood flow to that side of the brain is reduced and a stroke may result. In other cases, cholesterol particles from the atherosclerotic plaque may suddenly break off and enter the brain. In some people, these fragments come off from the heart and go to the brain. This often happens during a heart attack or an infection of the valves.[8] Other reasons include excessive narrowing of large vessels resulting from an atherosclerotic plaque and increased blood viscosity caused by some blood diseases. TIA is related to other medical conditions such as hypertension, heart disease (especially atrial fibrillation), migraine, cigarette smoking, hypercholesterolemia, and diabetes mellitus.

Alternative diagnoses
Other diagnoses may masquerade as a TIA: 1. Atypical migraine if visual symptoms occur such as perception of wavy or jagged lines or tiny specks of light and if a headache occurs.[citation needed] Typically a history of prior migraines is present.

2. Partial seizure in the parietal area of the brain can mimic TIA symptoms. 3. Glucose abnormalities can mimic TIAs. Ask about history of diabetes mellitus and loss of consciousness. 4. Electrolyte abnormalities 5. Hypertensive encephalopathy (headache, delirium, hypertension, cerebral edema) 6. Subdural hematoma (history of trauma, headache, loss of consciousness) 7. Brain tumor (mode of onset, progressive headaches, increased intracranial pressure) 8. Demyelinating disease 9. Conversion disorder

Prevention
A TIA may be prevented by changes in lifestyle; although most of these recommendations have no solid empirical data, most medical professionals believe them to be so. These include:

Avoiding smoking. Cutting down on fats and cholesterol to help reduce plaque build up. Eating a healthy diet composed of fruits and vegetables. Limiting sodium in the diet, which reduces blood pressure. Exercising regularly. Limiting alcohol intake. Maintaining a normal weight. Controlling blood pressure and keeping blood sugars under control.

Treatment
The mainstay of treatment following acute recovery from a TIA should be to diagnose and treat the underlying cause. It is not always immediately possible to tell the difference between a CVA (stroke) and a TIA. Most patients who are diagnosed at a hospital's emergency department as having suffered from a TIA will be discharged home and advised to contact their primary physician to organize further investigations. TIA can be considered as the last warning. The reason for the condition should be immediately examined by imaging of the brain. The initial treatment is aspirin, second line is clopidogrel, third line is ticlopidine. If TIA is recurrent after aspirin treatment, the combination of aspirin and dipyridamole is needed (Aggrenox). An electrocardiogram (ECG) may show atrial fibrillation, a common cause of TIAs, or other arrhythmias that may cause embolisation to the brain. An echocardiogram is useful in detecting thrombus within the heart chambers. Such patients benefit from anticoagulation. If the TIA affects an area supplied by the carotid arteries, an ultrasound (TCD) scan may demonstrate carotid stenosis. For people with a greater than 70% stenosis within the carotid artery, removal of atherosclerotic plaque by surgery, specifically a carotid endarterectomy, may be recommended. The blood vessel is opened up and the plaque is removed. The procedure is not

technically difficult but carries the potential complication of inducing a stroke. A stroke can occur during surgery or after the procedure. The chance of a stroke ranges from 14 percent.[9] Some patients may also be given modified-release dipyridamole or clopidogrel. To reduce recurrence of an attack, ACE inhibitor drugs are used. The aim is to prevent a sudden, significant drop in blood pressure, because blood pressure that is too low may increase ischemic injury due to low perfusion.

Medication
The use of anti-coagulant medications, heparin and warfarin; or anti-platelet medications such as aspirin may be warranted. Antiplatelet drugs prevent platelets from sticking to each other, thus making the blood thinner (i.e., less viscous). Thinning the blood helps to ensure that small particles do not form and travel to the brain. These drugs require frequent monitoring. These drugs also have side effects such as easy bruising, and bleeding from mild trauma.[10]

Risk factors

Family history of stroke or TIA substantially increases risk. People 55 years or older are at higher risk. Males have a slightly higher risk of TIA than females but females are more likely to die from a stroke. African Americans generally tend to have a high risk of dying from a stroke, chiefly due to high blood pressure and uncontrolled diabetes.[11]

Nervous System Organization

The nervous system integrates and monitors the countless actions occurring simultaneously throughout the entire human body. Therefore, every task, no matter how menial, accomplished by a person is a direct result of the components of the nervous system. These actions can be under voluntary control, like touching a computer key, or can occur without your direct knowledge, like digesting food, releasing enzymes from the pancreas, or other unconscious act It is difficult to understand all the complexities of the nervous system because the field of neuroscience has rapidly evolved over the past 20 years. Moreover, answers to new questions are being found almost daily. However, a thorough knowledge of the individual components of the nervous system and their functions will lead to a better understanding of how the human body works and facilitate the acquisition of knowledge in the future. The nervous system consists of two parts, shown in Figure 1 :

The central nervous system (CNS) consists of the brain and spinal cord. The peripheral nervous system (PNS) consists of nerves outside the CNS.

Figure 1Two parts of the nervous system.

Nerves of the PNS are classified in three ways. First, PNS nerves are classified by how they are connected to the CNS. Cranial nerves originate from or terminate in the brain, while spinal nerves originate from or terminate at the spinal cord. Second, nerves of the PNS are classified by the direction of nerve propagation. Sensory (afferent) neurons transmit impulses from skin and other sensory organs or from various places within the body to the CNS. Motor (efferent) neurons transmit impulses from the CNS to effectors (muscles or glands). Third, motor neurons are further classified according to the effectors they target. The somatic nervous system (SNS) directs the contraction of skeletal muscles. The autonomic nervous system (ANS) controls the activities of organs, glands, and various involuntary muscles, such as cardiac and smooth muscles. The autonomic nervous system has two divisions:

The sympathetic nervous system is involved in the stimulation of activities that prepare the body for action, such as increasing the heart rate, increasing the release of sugar from the liver into the blood, and other activities generally considered as fight-or-flight responses (responses that serve to fight off or retreat from danger). The parasympathetic nervous system activates tranquil functions, such as stimulating the secretion of saliva or digestive enzymes into the stomach and small intestine.

Generally, both sympathetic and parasympathetic systems target the same organs, but often work antagonistically. For example, the sympathetic system accelerates the heartbeat, while the parasympathetic slows the heartbeat. Each system is stimulated as is appropriate to maintain homeostasis.

anatomy
n physiology, the endocrine system is a system of glands, each of which secretes a type of hormone directly into the bloodstream to regulate the body. The endocrine system is in contrast to exocrine system, which secretes its chemicals using ducts. It derives from the Greek words endo (Greek ) meaning inside, within, and crinis (Greek ) for secrete. The endocrine system is an information signal system like the nervous system, yet its effects and mechanism are classifiably different. The endocrine systems effects are slow to initiate, and proglonged in their response, lasting for hours to weeks. The nervous system sends information very quickly, and responses are generally short lived. Hormones are substances (chemical mediators) released from endocrine tissue into the bloodstream

where they travel to target tissue and generate a response. Hormones regulate various human functions, including Metabolism, growth and development, tissue function, and mood. The field of study dealing with the endocrine system and its disorders is endocrinology, a branch of internal medicine. Features of endocrine glands are, in general, their ductless nature, their vascularity, and usually the presence of intracellular vacuoles or granules storing their hormones. In contrast, exocrine glands, such as salivary glands, sweat glands, and glands within the gastrointestinal tract, tend to be much less vascular and have ducts or a hollow lumen. In addition to the specialised endocrine organs mentioned above, many other organs that are part of other body systems, such as the kidney, liver, heart and gonads, have secondary endocrine functions. For example the kidney secretes endocrine hormones such as erythropoietin and renin. The endocrine system is made up of a series of glands that produce chemicals called hormones. A number of glands that signal each other in sequence is usually referred to as an axis, for example, the hypothalamic-pituitary-adrenal axis.

introduction
Diabetes mellitus type 2 formerly non-insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes is a metabolic disorder that is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency.[2] Diabetes is often initially managed by increasing exercise and dietary modification. If the condition progresses, medications may be needed. Unlike type 1 diabetes, there is very little tendency toward ketoacidosis though it is not unheard of.[3] One effect that can occur is nonketonic hyperglycemia. Long-term complications from high blood sugar can include increased risk of heart attacks, strokes, amputation, and kidney failure.

[edit] Signs and symptoms

The classic symptoms of diabetes are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), fatigue and weight loss.[4]

[edit] Cause
Type 2 diabetes is due to a combination of lifestyle and genetic factors.[5][6]. Recently, intrauterine growth restriction (IUGR) or prenatal undernutrition (macro- and micronutrient) was identified as another probable factor [7] A clue for this concept was the Dutch Hunger Winter and the pioneering work of Professor Barker

[edit] Lifestyle
A number of lifestyle factors are known to be important to the development of type 2 diabetes. In one study, those who had high levels of physical activity, a healthy diet, did not smoke, and consumed alcohol in moderation had an 82% lower rate of diabetes. When a normal weight was included, the rate was 89% lower. In this study, a healthy diet was defined as one high in fiber, with a high polyunsaturated to saturated fat ratio, and a lower mean glycemic index.[8] Obesity has been found to contribute to approximately 55% of cases of type 2 diabetes,[9] and decreasing consumption of saturated fats and trans fatty acids while replacing them with unsaturated fats may decrease the risk.[5] The increased rate of childhood obesity between the 1960s and 2000s is believed to have led to the increase in type 2 diabetes in children and adolescents.[10] Environmental toxins may contribute to recent increases in the rate of type 2 diabetes. A weak positive correlation has been found between the concentration in the urine of bisphenol A, a constituent of some plastics, and the incidence of type 2 diabetes.[11]

[edit] Medical conditions

There are many factors which can potentially give rise to, or exacerbate, type 2 diabetes. These include obesity, hypertension, elevated cholesterol (combined hyperlipidemia), and with the condition often termed metabolic syndrome (it is also known as Syndrome X, Reavan's syndrome, or CHAOS). Other causes include acromegaly, Cushing's syndrome, thyrotoxicosis, pheochromocytoma, chronic pancreatitis, cancer, and drugs. Additional factors found to increase the risk of type 2 diabetes include aging,[12] high-fat diets[13] and a less active lifestyle.[14] Subclinical Cushing's syndrome (cortisol excess) may be associated with type 1 diabetes.[15] The percentage of subclinical Cushing's syndrome in the diabetic population is about 9%.[16] Diabetic patients with a pituitary microadenoma can improve insulin sensitivity by removal of these microadenomas.[17] Hypogonadism is often associated with cortisol excess, and testosterone deficiency is also associated with type 2 diabetes,[18][19] even if the exact mechanism by which testosterone improves insulin sensitivity is still not known.

[edit] Genetics
There is also a strong inheritable genetic connection in type 2 diabetes: having relatives (especially first degree) with type 2 increases risks of developing type 2 diabetes substantially. In addition, there is also a mutation to the Islet Amyloid Polypeptide gene that results in an earlier onset, more severe, form of diabetes.[20][21] About 55 percent of type 2 diabetes patients are obese at diagnosis[22] chronic obesity leads to increased insulin resistance that can develop into type 2 diabetes, most likely because adipose tissue (especially that in the abdomen around internal organs) is a source of several chemical signals to other tissues (hormones and cytokines).

Other research shows that type 2 diabetes causes obesity as an effect of the changes in metabolism and other deranged cell behavior attendant on insulin resistance.[23] However, environmental factors (almost certainly diet and weight) play a large part in the development of type 2 diabetes in addition to any genetic component. This can be seen from the adoption of the type 2 diabetes epidemiological pattern in those who have moved to a different environment as compared to the same genetic pool who have not. Immigrants to Western developed countries, for instance, as compared to lower incidence countries of origins.[24] There is a stronger inheritance pattern for type 2 diabetes. Those with first-degree relatives with type 2 diabetes have a much higher risk of developing type 2 diabetes, increasing with the number of those relatives. Concordance among monozygotic twins is close to 100%, and about 25% of those with the disease have a family history of diabetes. Genes significantly associated with developing type 2 diabetes, include TCF7L2, PPARG, FTO, KCNJ11, NOTCH2, WFS1, CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX.[25][26] KCNJ11 (potassium inwardly rectifying channel, subfamily J, member 11), encodes the islet ATP-sensitive potassium channel Kir6.2, and TCF7L2 (transcription factor 7like 2) regulates proglucagon gene expression and thus the production of glucagon-like peptide-1.[27] Moreover, obesity (which is an independent risk factor for type 2 diabetes) is strongly inherited.[28] Monogenic forms, e.g., MODY, constitute 15 % of all cases.[29] Various hereditary conditions may feature diabetes, for example myotonic dystrophy and Friedreich's ataxia. Wolfram's syndrome is an autosomal recessive neurodegenerative disorder that first becomes evident in childhood. It consists of diabetes insipidus, diabetes mellitus, optic atrophy, and deafness, hence the acronym DIDMOAD.[30] Gene expression promoted by a diet of fat and glucose, as well as high levels of inflammation related cytokines found in the obese, results in cells that "produce fewer and smaller mitochondria than is normal," and are thus prone to insulin resistance.[31]

[edit] Pathophysiology