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Secondary prevention: After the biological onset of disease buy cheapest finasteride and finasteride hair loss cure japan, but before permanent damage sets in discount finasteride 1mg on line hair loss cure quick, we speak of secondary prevention buy 1 mg finasteride overnight delivery hair loss 11 year old. The objective here is to stop or slow the progression of disease so as to prevent or limit permanent damage, through the early detection and treatment of disease. Thertiary prevention: After permanent damage has set in, the objective of tertiary prevention is to limit the impact of that damage. The impact can be physical, psychological, social (social stigma or avoidance by others), and financial. Rehabilitation refers to the retraining of remaining functions for maximum effectiveness, and should be seen in a very broad sense, not simply limited to the physical aspect. Thus the provision of special disability pensions would be a form of tertiary prevention. Methods of Communicable Disease Control There are three main methods of controlling communicable diseases: 1. Man as reservoir: When man is the reservoir, eradication of an infected host is not a viable option. Instead, the following options are considered: 19 Communicable Disease Control Detection and adequate treatment of cases: arrests the communicability of the disease (e. Isolation is indicated for infectious disease with the following features: - High morbidity and mortality - High infectivity Quarantine: limitation of the movement of apparently well person or animal who has been exposed to the infectious disease for a duration of the maximum incubation period of the disease. Animals as reservoir: Action will be determined by the usefulness of the animals, how intimately they are associated to man and the feasibility of protecting susceptible animals. For example: Plague: The rat is regarded as a pest and the objective would be to destroy the rat and exclude it from human habitation. Reservoir in non-living things: Possible to limit man’s exposure to the affected area (e. Interruption of transmission This involves the control of the modes of transmission from the reservoir to the potential new host through: Improvement of environmental sanitation and personal hygiene Control of vectors Disinfections and sterilization 3. Protection of susceptible host: This can be achieved through: Immunization: Active or Passive Chemo-prophylaxis- (e. State the six important factors that involve the chain of communicable diseases transmission. Oral-oral transmission occurs mostly through unapparent fecal contamination of food, water and hands. As indicated in the schematic diagram below, food takes a central position; it can be directly or indirectly contaminated via polluted water, dirty hands, contaminated soil, or flies. Infectious agent Salmonella typhi Salmonella enteritidis (rare cause) Epidemiology Occurrence- It occurs worldwide, particularly in poor socio- economic areas. Annual incidence is estimated at about 17 million cases with approximately 600,000 deaths worldwide. In endemic areas the disease is most common in preschool and school aged children (5-19 years of age). Reservoir- Humans Mode of transmission- By water and food contaminated by feces and urine of patients and carriers. Flies may infect foods in which the organisms then multiply to achieve an infective dose. Incubation period –1-3 weeks 25 Communicable Disease Control Period of communicability- As long as the bacilli appear in excreta, usually from the first week throughout convalescence. About 10% of untreated patients will discharge bacilli for 3 months after onset of symptoms, and 2%-5% become chronic carriers. Relative specific immunity follows recovery from clinical disease, unapparent infection and active immunization but inadequate to protect against subsequent ingestion of large numbers of organisms. Clinical manifestation First week- Mild illness characterized by fever rising stepwise (ladder type), anorexia, lethargy, malaise and general aches. Severe illness with weakness, mental dullness or delirium, abdominal discomfort and distension. If no complications occur, patient begins to improve and temperature decreases gradually. Clinical manifestations suggestive of typhoid fever Fever- Sustained fever (ladder fashion) Rose spots- Small pallor, blanching, slightly raised macules usually seen on chest and abdomen in the first week in 25% of white people. Diagnosis Based on clinical grounds but this is confused with wide variety of diseases. Follow strictly enteric precautions: wash hands wear gloves teach all persons about personal hygiene 6. Observe the patient closely for sign and symptoms of bowel perforation erosion of intestinal ulcers sudden pain in the lower right side of the abdomen abdominal rigidity sudden fall of temperature and blood pressure 7. Education on handwashing, particularly food handlers, patients and childcare givers 3. Group A= Shigella dysentraie (most common cause) Group B= Shigella flexneri Group C= Shigella boydii Group D= Shigella sonnei Epidemiology Occurrence- It occurs worldwide, and is endemic in both tropical and temperate climates. Outbreaks commonly occur under conditions of crowding and where personal hygiene is poor, such as in jails, institutions for children, day care 29 Communicable Disease Control centers, mental hospitals and refugee camps. Two-thirds of the cases, and most of the deaths, are in children under 10 years of age. Reservoir- Humans Mode of transmission- Mainly by direct or indirect fecal-oral transmission from a patient or carrier. Transmission through water and milk may occur as a result of direct fecal contamination. Flies can transfer organisms from latrines to a non-refrigerated food item in which organisms can survive and multiply. Incubation period- 12 hours-4 days (usually 1-3 days) Period of communicability- During acute infection and until the infectious agent is no longer present in feces, usually within four weeks after illness. Diagnosis Based on clinical grounds Stool microscopy (presence of pus cells) Stool culture confirms the diagnosis Treatment 1. Infectious agent Entamoeba histolytica Epidemiology Occurrence- worldwide but most common in the tropics and sub-tropics. Mode of transmission – Fecal-oral transmission by ingestion of food or water contaminated by feces containing the cyst. Reservoir- Humans Mode of transmission- Person to person transmission occurs by hand to mouth transfer of cysts from feces of an infected individual especially in institutions and day care centers. Reservoir- Humans Mode of transmission- by ingestion of food or water directly or indirectly contaminated with feces or vomitus of infected person. Period of communicability- for the duration of the stool positive stage, usually only a few days after recovery. Antibiotics like tetracycline dramatically reduce the duration and volume of diarrhea resulting in early eradication of vibrio cholerae.

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Ruth Crocker—Thank you so much for sharing your wisdom with me during this long journey generic finasteride 5mg amex hair loss cure vitamin. We will overcome the debilitating effects of thyroid disease and help to ensure better outcomes for individuals yet to be diagnosed purchase generic finasteride canada hair loss hats. Across cultures buy generic finasteride on line hair loss cure news, the prevalence of thyroid disease is much higher among women than among men (Canaris, Manowitz, Mayor, & Ridgway, 2000; Cassidy, Ahearn, & Carroll, 2002). In fact, women have an estimated 1 in 7 chance of developing thyroid disease (Godfrey, 2007). A number of factors make proper diagnosis and treatment of thyroid disease challenging. In addition, as thyroid dysfunction produces symptoms similar to those of other disorders (e. In the face of such challenges, a doctor-patient relationship based on mutual trust and collaboration helps to ensure positive treatment outcomes (Houle, Harwood, Watkins, & Baum, 2007; Munch, 2004). In addition, effective communication between doctors and patients is critical in both the diagnosis and management of thyroid disease (Shimabukuro, 2008; Simmons, 2010). However, the culture of the medical profession, diagnostic bias, and gender differences in communication may interfere with doctor-patient discourse (Cheney & Ashcraft, 2007; Hamberg, Risberg, & Johansson, 2004; Hoffmann & Tarzian, 2001; Kaiser, 2002; Munch, 2004). An exploration of women’s experiences in the treatment of thyroid disease, especially relative to these three points, may contribute to better understanding on the part of doctors and thus more effective doctor-patient communication and relationships. Despite the pervasiveness of thyroid disease in women and the importance of the doctor-patient relationship in positive treatment outcomes, there is a gap in the literature regarding the treatment experiences of women diagnosed with thyroid disease, particularly regarding the doctor-patient relationship. Therefore, the purpose of this phenomenological study was to explore female thyroid patients’ experiences of treatment and the doctor-patient relationship. The phenomenological research approach was used, as it is designed to examine the meaning of experiences about a particular phenomenon (e. The theoretical perspectives used to guide data interpretation included feminism and social 3 constructivism. More specifically, the following issues were addressed in regard to their relationship with women’s treatment experiences: (a) the culture of the medical profession (see Kaiser, 2002; Thomas, 2001), (b) diagnostic bias (see Hamberg et al. The following paragraphs provide a review of the literature relevant to the study, followed by the problem statement, the purpose and nature of the study, research questions, conceptual framework, definition of terms, assumptions and limitations, and the significance of the study. Background of the Study The incidence of thyroid disease is higher than previously thought (Canaris et al. Across cultures, the prevalence of thyroid disease is much higher in women than men (Canaris et al. Approximately 1 out of every 7 women develops thyroid disease, and its prevalence increases with age (about 20% in women over age 60; Godfrey, 2007). The two predominant conditions resulting from thyroid disease are hyperthyroidism and hypothyroidism, with Grave’s disease and Hashimoto’s disease, respectively, as the most common causes (Zeitlin et al. In the United States, the most common cause of hyperthyroidism is Grave’s disease, an autoimmune form of thyroid disease (Bunevicius & Prange, 2006). Individuals with hyperthyroidism experience heat intolerance, hot flashes, absent menses, insomnia, decreased libido (Godfrey, 2007), rapid heartbeat, sweating, and tremors (Aslan et al. In the United States, the most common cause of hypothyroidism is Hashimoto’s disease, an autoimmune form of thyroid disease (Erdal et al. Individuals with hypothyroidism experience fatigue (Bono, Fancellu, Blandini, Santoro, & Mauri, 2004), lethargy, apathy, difficulty concentrating (Aslan et al. In extreme cases, the individual may experience slowing of thought processes, progressive cognitive impairment, hallucinations, and delusions (Bono et al. Furthermore, abnormalities in thyroid function present with symptoms similar to those of other disorders and can be mistaken for other conditions (Canaris et al. For example, hyperthyroidism and hypothyroidism are frequently misdiagnosed as anxiety and depressive disorders, respectively (Aslan et al. Postpartum thyroiditis, which affects more than 8% of women, is sometimes mistaken for depression (Fassier et al. In older patients, symptoms of hyperthyroidism and hypothyroidism often lead to inaccurate diagnoses of menopause or dementia (Godfrey, 2007; Shimabukuro, 2008). Thus, it is vital that physicians conduct a thorough assessment of their patients, including an ongoing discussion of symptoms, to ensure proper diagnosis and treatment. Although antithyroid drugs have been used for over 60 years, remission rates are variable, and relapses are frequent. However, some experts recommend the addition of T3 (liothyronine; name brand Cytomel) due to its antidepressant effects (Dayan, 2001; Joffe, 2006). As previously mentioned, proper treatment of thyroid disease is dependent upon accurate diagnosis. Misdiagnosis of thyroid disease delays treatment and can result in progressive psychological and physiological problems (Heinrich & Grahm, 2003; McDermott & Ridgway, 2001) including psychosis (Gaitonde, Rowley, & Sweeney, 2012; Heinrich & Grahm, 2003) and potential heart failure (Hak et al. These risks highlight the importance of an effective doctor-patient relationship in ensuring proper diagnosis and positive treatment outcomes. The treatment experiences of women with thyroid disease might be best examined from social constructionist and feminist viewpoints, as both worldviews emphasize individuals’ experiences in social contexts (Docherty & McColl, 2003; Fernandes, Papaikonomou, & Nieuwoudt, 2006; Hearn, 2009). From a social constructionist viewpoint, patients’ interpretations of their illness experience are important in understanding and treating illness. The feminist viewpoint suggests that female patients’ interpretations of their experiences are influenced by social constructs (e. Because social constructs come from patients, physicians, and social institutions (Hearn, 2009), women’s experiences with thyroid disease diagnosis and management may be influenced by the culture of the medical profession, diagnostic bias, and gender differences in communication. Culture of the Medical Profession In the Western medical profession, health-care practitioners are taught via the medical model to base their diagnostic and treatment decisions on “objective evidence” of disease (e. Additionally, as argued by Annandale and Clark (2000), health has become “marketed as a result of lifestyle choice” (p. In other words, the patient is totally responsible for his or her condition; if a person is overweight, then he or she must lack self-control. According to Vanderford, Stein, Sheeler, and Skochelak (2001), the traditional medical culture has encouraged physicians to behave in a paternalistic or authoritative manner when faced with differing treatment expectations from their patients. Traditional doctor-patient relationships are characterized by authoritarian and paternalistic approaches in which the physician controls the interview, makes a diagnosis, and chooses the treatment plan without the patient’s input (Ehrenreich & English, 2005; Vanderford et al. Research indicates that these types of doctor- patient interactions are related to lowered patient satisfaction and negative treatment outcomes (Bradley, Sparks, & Nesdale, 2001; Chrisler & Parrett, 1995; Copeland, Hudson Scholle, & Binko, 2003; Krupat, 1999; Stokes, Dixon-Woods, & Williams, 2006). Research indicates that physicians are more likely to interpret men’s symptoms as biological and women’s symptoms as psychosocial—that is, that women’s symptoms are a result of a mental, rather than physical, illness (Chrisler, 2001; Hamberg et al. In their study on the treatment experiences of women with chronic pain, Werner and Malterud (2003) purported that the medical profession encourages a normative, gendered view of illness, which results in a perceived need for women to work harder in order to be perceived as credible patients. As a result, female patients can become wary of honestly communicating their symptoms and the psychosocial effects of those symptoms (Peters et al. Gender Differences in Communication It has been argued that gender differences in medical treatment can be partially explained by gender differences in communication. Whereas men tend to describe their symptoms in a frank and confident manner, women often give generalized descriptions of their symptoms (Hamberg et al. Although these generalizations do not apply to all men and women, variations in communication patterns across genders have the potential to 9 influence how physicians and patients interact (Hamberg et al. With regard to conversation during medical consultations, evidence suggests that there is a significant disparity between the communication styles preferred by patients and those preferred by physicians.

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It has been proposed that interoceptive input has relevance beyond merely reporting the homeostatic “status” of the body order 5mg finasteride overnight delivery hair loss in men 39 s wearhouse coupons. In the model proposed by Craig and others generic 5mg finasteride with visa hair loss and hormone x, interoceptive signals appear to be integrated with emotional and cognitive input primarily in the anterior insula purchase discount finasteride on line hair loss 6 months post partum. This combined input is used continuously to create a sense of momentary “self” which can be consciously interpreted as happy, sad, healthy, ill, etc. Since visceral feedback from the gut and other body sites contributes to our conscious state of wellbeing, it then follows that the gut’s luminal organisms also have the opportunity to influence mood states like anxiety or depression [26, 27]. During an experimental task, when a brain region is more active compared to a baseline or control task, blood flow increases and thus a higher proportion of oxygenated hemoglobin is observed in that area. Alterations in resting brain function have also been described in patients with functional gastrointestinal disorders, which are believed to involve brain-gut axis dysfunction [36–38]. Whether these resting brain signal changes represent ongoing gastrointestinal input to the brain or persistent changes in the function of neural circuitry due to chronic disease is not yet known. Only one study to date has described functional brain changes in response to a probiotic intervention [29]. In this study healthy, normal weight women without any gastrointestinal symptoms, pain or psychiatric disorder, were randomized to treatment with a probiotic, a placebo dairy product or no treatment. This difference in brain activity was not correlated to any subject reports of mood or gastrointestinal symptoms. Evaluation of the microbiota in that study confirmed that the experimental probiotic could be identified in the stool of the probiotic ingesting subjects but did not show group specific changes in the overall architecture of the microbiota. This is consistent with other studies and suggests that microbial metabolites rather than overall microbial configuration may be the salient result of probiotic ingestion [42]. This initial study suggests that subtle changes in the gut contents can lead to measureable changes in brain function, even in the absence of a conscious awareness of the change. Differences in both white matter and gray matter have been identified in irritable bowel syndrome and functional dyspepsia, both of which are considered to be disorders of the brain- gut axis and which likely are accompanied by alterations in the gut microbiota [43– 51]. High resolution structural brain images can be used to produce global (whole- brain), regional, and voxel-level indices of gray matter density and volume as well as cortical thickness, surface area and mean curvature (Fig. Network analysis from graph theory has recently been applied to gray matter morphometry to demonstrate alterations in regional topology, providing strong evidence for exten- sive structural reorganization of cortical and subcortical regions previously impli- cated in altered brain responses to visceral pain stimuli and their expectation [43]. The biological substrate underlying grey matter changes may involve increased or decreased glial cells, changes in dendritic spines or synapses or less likely, neural degeneration. The next inner four rings depict the gray matter volume, surface area, cortical thickness, and degree of connectivity. The number of fiber tracks between regions is represented by the transparency of the line microbiota on gray matter structure is likely most profound during development, and has been shown in rodent models [56]. However, given that alterations in brain function and behavioral symptom changes occur in response to probiotic interven- tions in adults, it is likely that structural changes will follow. It has yet to be clearly defined whether the differences in brain structure in disorders of the brain-gut axis are a result of the chronic condition or a predisposing factor, though there is a great likelihood that both pathways occur. Associations between brain structure and microbiota profiles have not yet been described but provide an opportunity to better understand the interactions between the luminal contents and the brain. A radiotracer is injected and after the experiment the animal is sacrificed and the brain is cryosectioned to identify regional tracer uptake, allowing a very detailed view of the involved neural circuitry [58]. Using animal imaging in parallel with modula- tion of the microbiota is likely to inform human studies as animal studies allow for the control of more variables and ability to perform post-mortem studies of the brain. Modulation of gastrointestinal flora in rodents by using specific bacterial strains, antibiotics, or by using germ-free animals has shown associations with anxiety-like behavior across multiple paradigms [20, 21, 56, 59, 60]. Rodent models of anxiety-like behavior are well developed and show responses to pharmacological agents, such as selective serotonin reuptake inhibitors, indicating the presence of relevant shared core neural circuitry with humans. In humans, measures of anxiety and depression including clinical diagnosis, trait measures and psychological symptoms correlate 412 K. Similar to the findings in rodent models, the ingestion of a Bifidobacterium and Lactobacillius containing probiotic in healthy humans showed diminished psychological symptoms, including anxiety symptoms in a placebo controlled randomized clinical trial [64]. The central mechanisms through which these symptoms change can be probed with neuroim- aging, using symptom measures as covariates. In addition to looking at the inter- actions between psychological symptoms and brain function when modulating the microbiota in clinical trials, additional gastrointestinal measures such as intestinal permeability, immune activation, motility and visceral sensitivity will be useful in better elucidating gut to brain communication. Both the microbiome and the brain act within integrated networks for which classical hypothesis driven analytic approaches are not ideal. Agnostically applied multivariate analysis techniques are being used to identify neural networks to develop biomarkers of complex diseases, such as chronic pain, anxiety and depression. These approaches can be utilized to combine complex imaging datasets with genomic, metagenomic and metabolomic data to study the interaction between neural and microbial networks [67]. Since current evidence suggests that the gastrointestinal microflora are likely to play a role in the devel- opment and persistence of these disorders, it will be important to look at the interactions between brain phenotypes and the gut microbiome. In animals, we have the ability to meticulously manage the presence or absence of specific microorganisms, we are able to image the brain in both direct and indirect ways, and we can observe the effects of various environmental pressures on the developing animal. However, we are faced with the difficulty of translating the relevance of behavior from rodent models to humans, and must deal with the clear differences in the brain between species. He and others [69] have described the difficulties of the bench to clinical translation with a particular focus on interoception and pain processing, 18 Neuroimaging the Microbiome-Gut–Brain Axis 413 but similar arguments can be made for the study of the stress response, emotion and cognition. If an animal model, as Craig describes in the case of the rodent, lacks the anterior insular cortex, the site in which our subjective sense of physical wellbeing may arise, and if the basic pathways through which the visceral afferents commu- nicate with emotional and cognitive centers vary, then our animal models of complex phenomena must be interpreted with caution. Our access to the gut is limited and most data samples are collected non-invasively, via the stool. This allows us to examine the gut microbiome in broad strokes, but does not differentiate between the luminal and mucosal environment, much less local microenvironments or regional differ- ences throughout the gut [70, 71]. In humans the effects of diet, medications, and external stressors on microbiota content, gastrointestinal motility and immune function are difficult to account for even in the most carefully controlled experi- ments. Despite these concerns, the combination of human and animal imaging, using a translational or reverse-translational model [73–75] may prove to be the most effective and flexible strategy in evaluating the role of the gut microbiome in brain function, mood and cognition. The current focus on disorders of gastrointestinal disease, such as inflammatory or function bowel diseases, is already shifting to the study of anxiety and depression, metabolic diseases and neurologic disease. With this shift, incorporation of neuroimaging techniques will allow us to measure the rich con- nectivity between three complex systems: the microbiota, gut and brain. Nistal E et al (2012) Differences in faecal bacteria populations and faecal bacteria metabolism in healthy adults and celiac disease patients. Andoh A et al (2012) Multicenter analysis of fecal microbiota profiles in Japanese patients with Crohn’s disease. Asano Y et al (2012) Critical role of gut microbiota in the production of biologically active, free catecholamines in the gut lumen of mice. Barrett E et al (2012) Gamma-Aminobutyric acid production by culturable bacteria from the human intestine. Uribe A et al (1994) Microflora modulates endocrine cells in the gastrointestinal mucosa of the rat. Lesniewska V et al (2006) Effect on components of the intestinal microflora and plasma neuropeptide levels of feeding Lactobacillus delbrueckii, Bifidobacterium lactis, and inulin to adult and elderly rats.

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If there are factors that would lead to Driving may resume after 3 months an increased risk of recurrence order finasteride without a prescription hair loss cure yahoo, then 1 only if the cause has been identifed year off driving would be required 1mg finasteride sale revalid hair loss 90 capsules. If no cause has been identifed cheap 1 mg finasteride with mastercard hair loss 60 year old woman, the licence will be refused or revoked for 2 years. Blackout with seizure markers This category is for those where on the balance of probability there is clinical suspicion of a seizure but no defnite evidence. Depending on previous medical Depending on previous medical history, the standards for isolated history, the standards for isolated seizure or epilepsy will apply. Must not drive for 6 months following Must not drive for 12 months following a single episode and for 12 months a single episode and 5 years following following multiple episodes over multiple episodes over 5 years. If more than one episode of cough If more than one episode of cough syncope occurs within a 24 hour syncope occurs within a 24 hour period, this will be counted as a single period, this will be counted as a single event. However if the episodes of cough syncope are more than 24 hours cough syncope are more than 24 hours apart, these are considered as multiple apart, these are considered as multiple episodes. Primary/central hypersomnias – including narcolepsy and the narcolepsy/cataplexy syndrome For other causes of excessive sleepiness, see Chapter 8 (miscellaneous conditions). A licence may be reissued only when Relicensing may be considered subject there has been satisfactory symptom to specialised assessment and a control for at least 3 months before satisfactory objective assessment of being considered for re-licensing. For information on in-car driving assessments for those with a disability, see Appendix G (page 133). May drive as long as safe vehicle May drive as long as safe vehicle control is maintained at all times. If driving is not impaired and the The licence may specify a restriction to underlying condition is stable, licensing cars with certain controls. May drive as long as safe vehicle May drive as long as safe vehicle control is maintained at all times. If the individual’s condition is disabling If the individual’s condition is disabling and/or there is clinically signifcant and/or there is clinically signifcant variability in motor function, the licence variability in motor function, the licence will be refused or revoked. If driving is not impaired, licensing will If driving is not impaired, licensing will be considered subject to satisfactory be considered subject to satisfactory medical reports. Dizziness – liability to sudden and unprovoked or unprecipitated episodes of disabling dizziness Sudden is defned as ‘without suffcient warning to allow safe evasive action when driving’ and disabling is defned as ‘unable to continue safely with the activity being performed’. When satisfactory control of symptoms If there are sudden and disabling has been achieved, relicensing may be symptoms, the licence will be refused considered for restoration of the ’til 70 or revoked. If an underlying diagnosis is likely to cause recurrence, the patient must be asymptomatic and completely controlled for 1 year from an episode before reapplying for their licence. With adaptations, is no previous history of cardiovascular severe physical impairment may not be disease, a licence may be issued an obstacle to driving. If the level of stenosis is severe enough to warrant surgical or radiological intervention, the requirements for exercise or other functional test must be met – see Appendix C, page 121. May drive unless prophylactic treatment medication for seizures is prescribed, in which case an individual assessment will be required. Driving may resume after 6 months Driving will remain prohibited for provided there is no visual feld defect. If the tumour is associated with seizure, relicensing will not be considered until 10 years after surgery, provided these years are then free from seizures without epilepsy medication. Relicensing may be considered after 2 scans performed 12 months apart show no growth. Individual assessment will be considered if such lack of growth cannot be demonstrated. Driving may resume after 12 months provided there is no debarring residual impairment likely to affect safe driving. Driving may resume on recovery from Driving may resume on recovery from treatment. Malignant brain tumours – including metastatic deposits and pineal tumours The standards will apply to frst occurrence, recurrence and progression. Driving may resume 1 year after The licence will be refused or revoked completion of primary treatment. If these criteria cannot be met, a further 1 year off driving will be required following completion of primary treatment or following seizure. Driving may resume 2 years after the The licence will be refused or revoked completion of primary treatment. For those receiving immunotherapy and other molecular target treatments licensing will be considered by individual assessment. Relicensing may be considered 1 year The licence will be refused or revoked after completion of the primary treatment permanently. If these criteria cannot be met then driving must cease for 2 years following completion of primary treatment. For those receiving immunotherapy and other molecular target treatments licensing will be considered by individual assessment. Relicensing may be considered 1 year Relicensing may be considered after completion of the primary treatment 5 years after completion of the if the patient is otherwise well. If there has been a small subarachnoid haemorrhage but the bullet points above can otherwise be satisfed, and there is documented evidence of a full clinical recovery, driving may resume after 6 months. Subdural haematoma With any procedure, if another one is also undertaken (for example, a ventriculoperitoneal shunt and a craniotomy for a haematoma), the standards for that procedure also apply, and may take precedence. Resume driving on recovery if no At least 6 months off driving and will underlying lesion. Refusal or revocation: May be able to return to driving when risk of seizure has fallen to no greater than 2% per annum. Will need clinical confrmation of Relicensing may be considered after recovery and a documented normal 6 months provided comprehensive cerebral angiogram. Relicensing will not be considered until after at least 2 years and a specialist assessment. Annual seizure risk should be no greater than 2% and there should be no residual impairment likely to affect driving. Relicensing will not be considered until after at least 2 years and a specialist assessment. Annual seizure risk should be no greater than 2% and there should be no residual impairment likely to affect driving. Driving may resume following clinical Relicensing may be considered after recovery. Driving may resume following clinical Driving may resume following clinical recovery. Driving may resume after 1 month The licence will be refused or revoked provided there is no debarring residual permanently. There must be no debarring residual The licence will be refused or revoked impairment likely to affect safe driving.

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