Astelin

Paul E. Szmitko, MD

• Chief Medical Resident, Division of General
• Internal Medicine, St. Michael? Hospital
• University of Toronto
• Toronto, Ontario, Canada

A sizeable number of people with epilepsy will have known risk factors allergy medicine eyes purchase 10ml astelin with visa, but some of these are not currently amenable to preventive measures allergy testing panel buy astelin in india. These include cases of epilepsy attributable to cerebral tumours or cortical malformations and many of the idiopathic forms of epilepsy allergy testing jersey ci astelin 10 ml visa. One of the most common causes of epilepsy is head injury allergy shots bc buy astelin once a day, particularly penetrating injury. Pre vention of the trauma is clearly the most effective way of preventing post-traumatic epilepsy, with use of head protection where appropriate (for example, for horse riding and motorcycling) (34). Epilepsy can be caused by birth injury, and the incidence should be reduced by adequate perinatal care. Fetal alcohol syndrome may also cause epilepsy, so advice on alcohol use before and during pregnancy is important. Reduction of childhood infections by improved public hygiene and immunization can lessen the risk of cerebral damage and the subsequent risk of epilepsy (33, 34). Febrile seizures are common in children under five years of age and in most cases are benign, though a small proportion of patients will develop subsequent epilepsy. The use of drugs and other methods to lower the body temperature of a feverish child may reduce the chance of having a febrile convulsion and subsequent epilepsy, but this remains to be seen. These conditions are more prevalent in the tropical belt, where low income countries are concentrated. Elimination of the parasite in the environ ment would be the most effective way to reduce the burden of epilepsy worldwide, but education concerning how to avoid infection can also be effective. Most cases of epilepsy at the current state of knowledge are probably not preventable but, as research improves our understanding of genetics and structural abnormalities of the brain, this may change. Treatment gap Worldwide, the proportion of patients with epilepsy who at any given time remain untreated is large, and is greater than 80% in most low income countries (33, 34). The size of this treatment gap reflects either a failure to identify cases or a failure to deliver treatment. Inadequate case-finding and treatment have various causes, some of which are specific to low income countries. They include people’s attitudes and beliefs, government health policies and priorities (or the lack of them), treatment costs and drug avail ability, as well as the attitude, knowledge and practice of health workers. In addition, there is clear scarcity of epilepsy-trained health workers in many low income countries. The lack of trained personnel and a proper health delivery infrastructure are major problems, which contribute to the overall burden of epilepsy. This situation is found in many other resource-poor countries and is usually more acute in rural areas. The lack of trained specialists and medical facilities needs to be seen in the context of severe deficiencies in health delivery that apply not only to epilepsy but also to the whole gamut of medical conditions. Training medical and paramedical personnel and providing the necessary investigatory and treatment facilities will require tremendous effort and financial expenditure and will take time to achieve. The aim should be to provide high standards of epilepsy care with equitable access to all who need them throughout the world. A huge effort is required to equalize care for people with epilepsy around the world. Improvement of the care delivery system and infrastructure alone are not a sufficient strategy but need to be supplemented by education of patients, their families and the general public. So far, research has been unsuc cessful in developing effective strategies capable of preventing the development of the pathogenic process, set in motion by different etiological factors, that leads ultimately to chronic epilepsies (38). To do so, it is important to take advantage of the results that are continuously being made available to the scientific community thanks to the synergy of basic and clinical multidisciplinary research. This means that the clinical applicability of neurobiological results should be evaluated, the way in which the new information can be translated into diagnostic and therapeutic terms should be assessed, and ad hoc guidelines and recommendations should be produced accordingly. In elaborating their health-care strategies, regional and national communities should not simply refer to the available scientific information, but should also contribute to it by means of their own 64 Neurological disorders: public health challenges original investigations. This is mandatory if they are to meet specific local requirements taking into account the socioeconomic situations in which health-care policy is to be formulated. A specific project for collaborative studies involving developed and developing countries is part of the triennial action plan of the Global Campaign Against Epilepsy. The main point here is that research is not a matter of technology; rather, it is the result of an intellectual attitude aimed at understanding and improving the principles upon which every medical activity should be based. Therefore, everybody whose work concerns epilepsy can and should contribute to the advancement of epileptology to the benefit of the millions of human beings suffering from epilepsy, no matter how advanced the technological context of his or her current work. The need for an integrated, multidisciplinary approach to epilepsy care prompted several countries to organize annual epilepsy courses for neurologists, general practitioners, technicians and nurses at national level. The aim of the train the-trainers courses is to turn experienced personnel into qualified teachers of epileptology. It significantly contributes to raising the profile of epilepsy care across Europe and is now being implemented in other regions. European Epileptology Certification can be obtained by completing an 18-month educational programme based on periods of training in selected institutions that allow the accumulation of credits. Some mod ules have been completed and successfully tested: the course on genetics of epilepsy has already been evaluated (40). An annual residential Epilepsy Summer School for young epileptologists from all over the world exists at Venice’s International School of Neurological Sciences; since 2002, it has trained students from 64 countries. The interaction between students and teachers and among the students themselves resulted in several ongoing international collaborative projects that are further contributing to raising the profile of epilepsy care in several developing areas (41). The theoretical teach ing, based either on residential courses or distance education systems, includes an interactive discussion of clinical cases and practical training programmes in qualified epilepsy centres. A further effort is needed to expand exchange programmes for visiting students from economically disadvantaged countries. The Campaign aims to provide better information about epilepsy and its consequences and to assist governments and those concerned with epilepsy to reduce the burden of the disorder. The goals of the conferences were to review the present situation of epilepsy care in the region, to identify the country’s needs and resources to control epilepsy at a community level, and to discuss the involvement of countries in the Campaign. As a result of these consultations, Regional Declarations summarizing perceived needs and proposing actions to be taken were developed and adopted by the conference participants. In order to make an inventory of country resources for epilepsy worldwide, a questionnaire was developed by an international group of experts in the field. On the basis of the data collected through this questionnaire, regional reports were developed. These reports provide a panoramic view of the epilepsy situation in each region, outline the various initiatives that were taken to address the problems, define the current challenges and offer appropriate recommendations (32, 42). The next logical step in the assessment of country resources was the comprehensive analysis of the data. One of the main activities aiming to assist countries in the development of their national pro grammes on epilepsy is the initiation and implementation of demonstration projects. The ultimate goal of these projects is the development of a variety of successful models of epilepsy control that may be integrated into the health-care systems of the participating countries and regions. In general terms, each demonstration project has four aspects: assessing whether knowledge and attitudes of the population are adequate, correcting misin formation and increasing awareness of epilepsy and how it can be treated; assessing the number of people with epilepsy and estimating how many of them are appro priately treated; ensuring that people with epilepsy are properly served by health personnel equipped for their task; analysing the outcome and preparing recommendations for those who wish to apply the find ings to the improvement of epilepsy care in their own and other countries. Difficulties with availability of or access to treatment (the treatment gap) may seriously impair the prognosis of epilepsy and aggravate the social and medical consequences of the disease. Systematic review and meta-analysis of incidence studies of epilepsy and unprovoked seizures. The incidence of epilepsy and unprovoked seizures in Rochester, Minnesota, 1935–1984. Socioeconomic characteristics of childhood seizure disorders in the New Haven area: an epidemiologic study. Comparative epidemiology of epilepsy in Pakistan and Turkey: population-based studies using identical protocols. Epilepsy in developing countries: a review of epidemiological, sociocultural, and treatment aspects. The cost of epilepsy in the United States: an estimate from population-based and survey data. The cost of epilepsy in the United Kingdom: an estimation based on the results of two population-based studies. Cost-effectiveness of first-line anti-epileptic drug treatments in the developing world: a population-level analysis. Report of the Ad Hoc Committee on Health Research related to Future Intervention Options.

Apparently allergy symptoms lungs purchase cheapest astelin, the lowing allergy testing columbia mo order genuine astelin on line, hearing allergy rhinitis treatment 10 ml astelin otc, eye movements allergy medicine dogs can take cheap astelin, and facial expression and extra sugar in my blood was breaking down small cap sensation. Tere are also a number of cranial nerve nuclei in illaries in my feet, which was affecting sensory nerves the pons (Saladin, 2007; Zemlin, 1998). He was unsure whether it would get better or not because it depended on how long I had had diabetes the Midbrain and the damage that had been done. Fortunately, most The midbrain lies inferior to the diencephalon and supe of the neuropathy has disappeared because my diabe tes is now under control. Middle Nucleus cuneatus Central canal Spinocerebellar tract Central gray Nucleus ambiguus Spinothalamic tract Medial longitudinal fasciculus Corticospinal tract Medial lemniscus C. Each peduncle has a posterior part source of a sound and our startle response to a loud noise. Destruction of dopamine Tere are 12 pairs of cranial nerves that control sensory, spe producing cells can cause progressive neurological move cial sensory, motor, and parasympathetic functions of the ment disorders, like Parkinson’s disease. This branch also carries proprioceptive information from the Cranial Nerves for Articulation Cranial nerves involved muscles of chewing to the brainstem. Tese will be information is important for jaw opening and closing during discussed in this section. The extracranial branch inner goid), and protrude the mandible (lateral pterygoid muscle). As far as sensory function, the ophthalmic branch relays sensation from the upper face. Orbicularis oris (constricts oral opening) back to the brainstem and cerebral cortex. Risorius (retracts lip corners) branch carries sensory information from the nose, mouth. Buccinator (moves food onto molars for grinding) lower face, auditory meatus, and meninges. Tese connections mean that the pharyngeal branch has motor, sensory, special sensory, and parasympathetic controls pharyngeal constriction as well as palatal elevation. Only its motor and sensory functions are notable Palatal elevation is a key feature in speech and swallowing. It innervates the stylopharyn For speech, the palate elevates, allowing for the production geus muscle, a muscle that helps to elevate the pharynx and of non-nasal sounds. The information from the Eustachian tube, pharynx, and tongue cranial portion joins the vagus nerve and becomes indis back to the brainstem and the sensory areas of the cerebral tinguishable from it, thus playing a role in pharyngeal and cortex. The tongue is crucial The vagus nerve (X) has motor, sensory, special sensory, for chewing, swallowing, and speech. Relevant for speech are its of articulation and consists of both intrinsic and extrinsic motor and sensory functions. Vertical (pulls tongue down to mouth foor) The extrinsic tongue muscles work to move the tongue. Its internal branch relays sensory information from the thyrohyoid membrane, a broad layer of tissue that runs from the hyoid bone down to the thyroid cartilage. Tere are also a number of extrinsic laryngeal muscles that elevate and depress the larynx. Tese same muscles are also used for the oral preparatory and oral phases of the normal swallow. As air passes leading to pharyngeal constriction, which is experienced as upward during expiration it vibrates the vocal folds, which in a squeezing sensation in the throat during swallowing. Superior pharyngeal constrictor (narrows pharyngeal adduction, abduction, tension, and relaxation of the vocal diameter) cords, thus playing a critical role in speech production. The trigeminal also carry auditory information to the thalamus’s auditory center, dilates the Eustachian tube, thus helping to equalize pressure the medial geniculate body, which then is projected to the between the middle ear and the environment. It is also known as the vestibulocochlear nerve, a Cerebral Peduncles The cerebral peduncles or crus cere name that describes its branches, one for hearing and one for bri are bulges on the ventral side of the midbrain. The acoustic or cochlear branch transmits auditory eral corticospinal and corticobulbar tracts run through these information from the cochlea in the inner ear to the pons/ bulges, the lateral corticobulbar tract being important for medulla. Between the peduncles and the tegmen the body’s position in space via the semi-circular canals to tum is the substantia nigra, which produces dopamine. Internal Organization of the Brainstem Ventral Pons The corticopontine fbers originate from the motor cortex, pass through the cerebral peduncles, and Tegmental Regions input into ventral pons nuclei. Projections from the ventral The tegmentum is the core of the brainstem, which is contin pons then course to the cerebellum. The non nuclei’s close connection the cerebellum, it is thought this tegmental areas are not continuous and lie near the surface connection plays a role in motor movement error correc of the brainstem. Error correction is an important aspect of learning formation, inferior olivary complex, and red nucleus. This would be an important skill for learning to speak both a frst and a second Reticular Formation Nuclei are groups of specialized language. The nuclei of the reticular formation are scattered throughout the tegmentum (Figure 5-9B). The reticular formation regulates many One disorder that can result from medullar damage is aspects of human experience, including consciousness, the Wallenberg syndrome (also called lateral medullary syn sleep–wake cycle, cardiovascular functions, and respiration. It is typically caused by a stroke involving one of the arteries that supplies blood to the medulla. Patients with this Inferior Olivary Nucleus The inferior olivary nucleus condition experience contralateral loss of pain and temper (not to be confused with the superior olivary nuclei related ature in the body, ipsilateral loss of pain and temperature in to hearing) is a bulge on the medulla (Figure 5-8). It receives the face, vertigo, ataxia, paralysis of the ipsilateral palate and axons from the cerebral cortex and afer processing the vocal cord, and dysphagia. Its connection to the quent and violent hiccups that can last for weeks and make cerebellum suggests it plays a role in the control and coordi speaking, eating, and sleeping difcult. Its name comes from the fact that it is to patient, with some making a complete recovery, whereas pink due to the presence of iron. Basically, the person is locked inside his or her body, unable Nontegmental Regions to move, but is cognitively intact. The person cannot speak or As mentioned earlier, nontegmental areas of the brainstem swallow, and somatosensory abilities may or may not remain are found at or near the brainstem’s surface rather than deep intact. Tree nontegmental areas will be briefy cially establishing a system for communication. Dorsally, The memoir The Diving Bell and the Butterfy by it has two hills: the superior colliculi and the inferior col Jean-Dominique Bauby (1998), as well as the flm of the same liculi. The superior colliculi are connected to vision and the title, familiarized the general public with this condition. Cerebellum the Midbrain Midbrain damage can result in Weber’s or Benedikt’s syn Midbrain drome. Weber’s syndrome is characterized by contralateral Brainstem Pons hemiplegia and ipsilateral oculomotor paralysis with ptosis. Spinal cord Benedikt’s syndrome is similar to Weber’s but results in con tralateral hemiparesis and ataxic tremor. The Cerebellum The two hemispheres are separated by a mound of tissue called Anatomy of the Cerebellum the vermis. Each hemisphere is made up of a central core of white matter and a surface of gray matter. Tere are three looks like a piece of caulifower in that it has numerous wrin of these bundles, the inferior, middle, and superior cerebellar kles, called folia, that give the cerebellum enormous surface peduncles. The cerebellum also has lobes mainly aferent information, whereas the superior peduncle similar to the cerebral cortex. It also has two hemispheres like Cerebellar Function the cerebral cortex, a right hemisphere and a lef hemisphere. Functionally, the cerebellum is like a second brain, monitor ing sensory input from a wide array of sensory sources and Vermis Anterior lobe integrating this feedback into motor movement. The cerebellum participates in the plan ning, monitoring, and correction of motor movement using all the sensory input it collects. Cerebellar control is ipsilat eral as compared to the cerebral cortex, where the majority of control is contralateral in nature. The function of the cerebellum can be tested through a Posterior lobe variety of methods. The fnger–nose–fnger method involves Cerebellum (dorsal view) a person touching the examiner’s fnger, then his or her own nose, and then the examiner’s fnger again. This is a person’s ability to make rapid, alternating movements with either the fngers or the mouth. Folia Cerebellar Disorders Cerebellum (parasagittal section) All cerebellar disorders are motor in nature.

The sensory system itself can be dam aged and become the source of continuous pain allergy fatigue purchase astelin 10 ml fast delivery. Chronic neuropathic pain has no physical protective role as it continues without obvious ongoing tissue damage allergy testing prep buy cheap astelin 10 ml line. Pain without any recognizable tissue or nerve damage has its cause classified as idiopathic pain kellogg allergy shots cheap 10ml astelin with mastercard. A clinician’s duty is to diagnose allergy treatment using cold laser for drug withdrawal generic astelin 10ml with mastercard, treat and support pain patients, which means the identification of pain type(s) and their causative disease(s). It is also to provide adequate treatment aimed at the cause of the pain and symptomatic relief which should include psychosocial support. As the definition of pain reveals, pain has both a physical and a psychological element. The latter plays an important part in chronic pain disorders and their management. Adequate pain treatment is a human right and organization of it involving all its dimensions is the ethical and legal duty of society, health-care professionals and health-care policy-makers. Pain can also be an indirect conse quence of a nervous disease when it causes secondary activation of pain pathways. Examples of these types of pain include musculoskeletal pain in extrapyramidal diseases such as Parkinson’s disease, or deformity of joints and limbs due to neuropathies or infections. Pain begins frequently as an acute experience but, for a variety of reasons — some physical and often some psychological — it becomes a long-term or chronic problem. Pain directly caused by diseases or abnormalities of the nervous system Neuropathic pain In contrast to nociceptive pain which is the result of stimulation of primary sensory nerves for pain, neuropathic pain results when a lesion or disruption of function occurs in the nervous system. Neuropathic pain is often associated with marked emotional changes, especially depression, and disability in activities of daily life. Painful diabetic neuropathy and the neuralgia that develops after herpes zoster are the most frequently studied peripheral neuropathic pain conditions. Diabetic neuropathy has been estimated to afflict 45–75% of patients with diabetes mellitus. About 10% of these develop painful diabetic neuropathy, in particular when the function of small nerve fibres is impaired. Pain is a normal symptom of acute herpes zoster, but disappears in most cases with the healing of the rash. In 9–14% of patients, pain persists chronically beyond the healing process (postherpetic neuralgia). Neuropathic pain may develop also after peripheral nerve trauma as in the condition of chemotherapy-induced neuropathy. The frequencies of many types of peripheral neuropathic pain are not known in detail but vary considerably because of differences in the frequency of underlying diseases in different parts of the world. While pain caused by leprosy is common in Brazil and parts of Asia, such pains are exceedingly rare in Western parts of the world. Because of an explosion in the frequency of diabetes as a result of obesity in many industrialized countries and in South-East Asia, the likely result of this will be an increase in painful diabetic neuropathy within the next decade. Central neuropathic pain, including pain associated with diseases of the spinal cord. Central post-stroke pain is the most frequently studied central neuropathic pain condition. Two thirds of patients with multiple sclerosis have chronic pain, half of which is central neuropathic pain (3). Damage to tissues of the spinal cord and, at times, nerve roots, carries an even higher risk of leading to central neuropathic pain (myelopathic pain). The cause may lie within the cord and be intrinsic, or alternatively, be extrinsic outside the cord. Intrinsic causes include multiple scle rosis and acute transverse myelitis, both of which may result in paraplegia and pain. In certain developing countries, for example in sub-Saharan Africa, intrinsic damage may be attributable to neurotoxins — as in the case of incorrectly prepared cassava, which leads to tropical spastic neurological disorders: a public health approach 129 paresis. Lathyrism resulting from consumption of the grass pea (Lathyrus sativus) may cause a spinal disorder and, in both cases, pain is a significant symptom (see also Chapter 3. Other causes include compressive lesions, for example tumours and infections, especially tuberculosis and brucellosis. Pain indirectly caused by diseases or abnormalities of the nervous system Pain arises as a result of several distinct abnormalities of the musculoskeletal system, secondary to neurological disorders. These can be grouped into the following categories: musculoskeletal pain resulting from spasticity of muscles; musculoskeletal pain caused by muscle rigidity; joint deformities and other abnormalities secondary to altered musculoskeletal function and their effects on peripheral nerves. Pain caused by spasticity Pain caused by spasticity is characterized by phasic increases in muscle tone with an easy pre disposition to contractures and disuse atrophy if unrelieved or improperly managed. In developed countries, the main causes of painful spasticity are strokes, demyelinating diseases such as multiple sclerosis, and spinal cord injuries. With an ageing population, especially in the industrial ized countries, and rising numbers of road traffic accidents, an increase in these conditions, and therefore pain, is to be expected in the future. Strokes and spinal cord disease are also major causes of spasticity in developing countries, for example stroke is the most common cause of neurological admissions in Nigeria. Pain caused by muscle rigidity Pain can be one of the first manifestations of rigidity and is typically seen in Parkinson’s disease, dystonia and tetanus. Apart from muscle pain in the early stages of Parkinson’s disease, it may also occur after a long period of treatment and the use of high doses of L-Dopa causing painful dystonia and freezing episodes. Tetanus infection, common in developing countries, is characterized by intense and painful muscle spasms and the development of generalized muscle rigidity, which is extremely painful. During intense spasm, fractures of spinal vertebrae may occur, adding further pain. Pain caused by joint deformities A range of neurological disorders give rise to abnormal stresses on joints and, at times, cause deformity, subluxation or even dislocation. For example “frozen shoulder” or pericapsulitis occurs in 5–8% of stroke patients. Disuse results in the atrophy of muscles around joints and various abnormalities giving rise to pain, the source of which are the tissues lining the joint. In addition, deformities may result in damage to nerves in close proximity resulting in neuropathic pain of the “evoked” or spontaneous type. The literature does not give data for the prevalence and incidence of the pain associated with the disorders mentioned. The symptoms exceed both in magnitude and duration those which might be expected clinically given the nature of the causative event. Other features of the syndrome include local oedema or swelling of tissues, abnormalities of local blood flow, sweating (autonomic changes) and local trophic changes. They are a cause of significant psychological and psychiatric disturbance, and treatment is a major problem. Headache and facial pain Any discussion of pain arising from disorders of the nervous system must include headache and facial pains: these conditions are discussed in Chapter 3. They have been the subject of considerable research and been carefully classified by the International Headache Society. Epidemiological studies have focused primarily on migraine and tension-type headaches (primary headache disorders). Pain is a subjective experience but physiological changes that accompany it may be measured: they include changes in heart rate, muscle tension, skin conductivity and electrical and metabolic activity in the brain. These measures are most consistent in acute rather than chronic pain and they are used primarily in laboratory studies. Clinically, pain assessment includes a full history of the development, nature, intensity, location and duration of pain. The use of words as descriptors of pain have permitted the development of graded descriptions of pain severity. For example, mild pain, moderate pain, severe pain and very severe pain, to which numerical values may be attached (1–4), may be graded on a numerical scale from 0 to 4 indicat ing the level of pain being experienced. In clinical practice, however, there is widespread use of a 0–10 scale, a visual analogue scale, which is easy to understand and use and is not affected by differences in language. Such measures are often repeated at intervals to gain information about the levels of pain throughout the day, after a given procedure or as a consequence of treatment. More sophisticated verbal measures use groups of words to describe the three dimensions of pain, namely its sensory component, the mood-related dimension and its evaluative aspect. This technique was devised by Melzack and others and is best seen in the Short-Form McGill Pain Questionnaire (5). Often because of age, not having English as a first language or as a result of some form of mental impairment, the scale cannot be used.

More complex activities such as managing the bank account allergy shots near me purchase cheapest astelin, organising the household or arranging travel allergy testing nuts purchase astelin overnight, are impaired first allergy symptoms 7 months order astelin, while basic activities such as dressing allergy shots for dust mites order astelin with visa, grooming, preparing simple meals, eating, or using the toilet are affected later [5]. This definition of dementia is very broad and covers a number of different clinical presentations which depend primarily on the cerebral localisation of the underlying disease. The temporo-parietal type is characterised by impairments of memory, orientation, language, recognition and handling of objects [23]. Changes of personality and social conduct as well as impairment of judgement and problem solving, are the hallmarks of the frontal type which may be associated with either apathy or agitation [6]. In the subcortical type, slowing of information processing and changes of affect are associated with frontal symptoms [13]. It is important to note that the current definition links dementia to the presence of a significant impairment in activities of daily living, i. In most diseases, which ultimately lead to dementia, this stage of clinical severity is only reached when a significant degree of brain damage has accumulated. Therefore, the goal of early diagnosis is to identify these diseases before dementia has developed [16]. Dementia must be distinguished from normal ageing and from two other symptom patterns (or syndromes), which occur relatively frequently in the elderly: amnesia and delirium. The deterioration of some cognitive abilities which can be associated with normal ageing is very slow and never shows the observable decline within one or two years as it is seen in dementia [17]. Furthermore, in normal ageing there is no significant loss of 12 Alzheimer Europe Rare Forms of Dementia Project activities of daily living due to impaired cognition. Amnesia is a state of relatively isolated memory impairment in the absence of significant changes in personality, social conduct, and emotional control [8]. The characteristics of delirium are rapid onset, fluctuating course, and clouding of consciousness which becomes apparent in a reduced ability to focus and shift attention. Patients are usually disoriented: they may have vivid hallucinations, delusions, and agitation [9]. Dementia can be caused by a large number of diseases some of which affect only the brain while others affect the body as a whole. For the purposes of the present documentation we have classified these diseases into six main categories (neurodegenerative, infectious, traumatic, toxic, cerebro-vascular and metabolic). They are characterised by a progressive loss of nerve cells and synaptic connections. The second largest category of dementia causes comprises diseases of brain blood vessels. By reducing or cutting off blood supply they result in large or small infarcts as well as in demyelinisation of the fibers connecting nerve cells [18]. Compared to these two categories, traumatic, toxic, infectious, and metabolic causes of dementia are rare. Nevertheless these categories are important because in several of these diseases dementia may be reversible by adequate treatment [22]. As mentioned above, neuro-degenerative and small-vessel cerebro-vascular diseases which account for the majority of dementias are gradually progressive. Over extended periods of their course they are clinically silent because the brain can compensate a remarkable amount of pathology. Only when nerve cell and synaptic loss has reached a certain threshold symptoms become apparent. Initial symptoms consist in minor impairments of memory, attention, and executive functions, or in slight changes of personality, social conduct, and initiative. These symptom patterns represent a pre dementia stage of a number of diseases and are termed „mild cognitive impairment“ [14]. Different definitions of mild cognitive impairment have been proposed, some of which focus on memory impairment [15] while others are broader [4]. Follow-up studies have consistently demonstrated that patients with an amnestic type of mild cognitive impairment are likely to develop dementia at an annual rate of 12 to 15 % [12]. For the affected individual having dementia is associated with a progressive loss of abilities, personal autonomy, social roles and gratifications. Quality of life is further reduced by non-cognitive symptoms including depression, agitation, anxiety, delusions, illusionary misidentifications, and hallucinations. At later stages of dementia, physical symptoms such as epileptic seizures, difficulty swallowing, and gait disorder also occur. The management of dementia must therefore aim at maintaining cognition as well as 13 Alzheimer Europe Rare Forms of Dementia Project activities of daily living and physical well-being for as long as possible, and to minimise non-cognitive symptoms, combining pharmacological and non-pharmacological treatment strategies. For family members living with a demented person means a heavy and continuous burden which significantly increases the probability of psychological and physical morbidity [1]. The loss of a loved one, a change of roles and responsibilities, and withdrawal of relatives and friends all contribute to caregiver burden. Non-cognitive symptoms are more closely associated with caregiver distress than impairment of cognition or loss of activities of daily living [2]. Hence, providing advice and support to caregivers and improving their ability to cope with disease-related problems is another essential part of dementia management [19]. Brodaty H, Luscombe G (1998) Psychological morbidity in caregivers is associated with depression in patients with dementia. Variations in definitons and evolution of nondemented persons with cognitive impairment. Rockwood K, Bowler J, Erkinjuntti T, Hachinski V, Wallin A (1999) Subtypes of vascular dementia. This information is processed in the brain by nerve cells, analysed and integrated with our own information, our knowledge and our experience. The result of the integration generates an adapted response, an action if necessary, a storage in our memory if the information is interesting or important. All this work is performed by different specialised nerve cells, also known as neurons, that are gathered in specific neuronal populations that have different and specialised roles and location. Their function is to transport and to store the information (memory), or to trigger the activity of other cells (muscle fibers for example). The information is transported along neuronal extensions of nerve cells, called the axons. Information can jump and circulate to another neuron via a “synapse”, which is located at the end of the axon. The synapse bridges the gap between each neuron and allows the next neuron in the chain to be activated. All the information, received as micro-electric currents, is processed, analysed, integrated and then the resulting information is delivered to the appropriate neuron, via a synapse, for a specific task. For example, for vision, the eyes receive the visual information through numerous and specialised photoreceptors distributed on the retina. The visual information is then transported along axons, via a subset of neuronal population (colliculus), towards the occipital cortex. The information corresponding to the image is then transported to other brain areas to be analysed. The picture of the screen on the occipital pole (which is a primary visual area) is then analysed in secondary visual areas, and recognised as a specific object such as “an apple” for example. This recognition is the result of a comparison of the shape of the object with our knowledge of objects stored in the secondary visual areas (occipital regions around the occipital pole). Then the information is processed progressively (but very rapidly) by all other brain areas, at higher intellectual levels: the apple is recognised as a “golden” apple. If you do not like apples, you will be reminded of this by other brain areas involved in feelings and emotions, namely the limbic system. If you grab 16 Alzheimer Europe Rare Forms of Dementia Project the apple, you will activate your motor brain areas located in the upper part of the frontal cortex that will activate the nerves of your arms, then the muscles to grab the apple. In fact, the functioning of the brain is logical and easy to understand in its main lines. But to work properly, the mechanisms at the molecular levels are extremely complex and well regulated. The transmission of the information from one nerve cell to the other the synapse is a specialised neuronal ending that connects one neuron to another one in order to relay information. When the micro-current arrives at the synapse level, it releases a special molecule, known as neuromediator or neurotransmitter, that activates the other neuron, which in turn transmits the information. Drugs that stimulate the production of acetyl-choline are commercialised (Aricept , Exelon , Reminyl ) for use in the treatment of Alzheimer’s disease.

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