Search Results

Recent advances in imaging technology provide new means of assessing atypical parkinsonian patients and offer both clinicians and researchers more accurate differential diagnoses than history and exam alone. The optimal technique is one that provides high discriminatory power between atypical parkinsonian syndromes (e.g. multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration, diffuse Lewy body disease) in individual patients presenting with early symptoms, ideally without requiring significant technical expertise. Such techniques are invaluable to researchers, and eventually clinicians, as new treatments are developed, tested, and ultimately made available for patients with atypical parkinsonian syndromes.

This chapter provides an in-depth discussion of how current neuroimaging techniques can aid the clinician in the diagnosis of patients with parkinsonian symptoms. Although clinical assessment and structural imaging can rule out secondary causes, several functional imaging techniques are available to help the clinician with a critical diagnostic question—whether the symptoms are due to idiopathic Parkinson’s disease (PD) versus an alternative parkinsonian syndrome. If the symptoms are due to an alternative non-PD syndrome, the clinician must determine which one. The chapter reviews how the presenting symptom complex and the differential diagnosis can be used to choose the most informative imaging strategy. Clinical applications of imaging for parkinsonism are discussed in terms of the predominant presenting features, such as akinetic rigidity, tremor, or cognitive dysfunction (dementia). New metabolic imaging data on the use of brain networks to classify individual subjects are also discussed.

Transcranial sonography (TCS) has recently been introduced as an ancillary tool for the diagnostic workup of idiopathic Parkinson’s disease (PD) and related disorders. This approach has found particular use in individuals with early/mild disease manifestations in whom the clinical diagnosis in uncertain. Current research focuses on elucidating the pathophysiological basis of ultrasound changes, and improving the diagnostic accuracy of this versatile and promising imaging tool. The Chapter provides essential information concerning TCS methodology and its limitations, as well as the use of this approach in the differential diagnosis of idiopathic PD, atypical parkinsonian syndromes, and related disorders such as vascular parkinsonism and essential tremor.

Like everyone else, physicians take shortcuts when processing complex information. Unfortunately, mistakes in diagnosis often result. This chapter applies what we know about cognitive errors to better understand the likelihood that a baby who presents with one or more triad symptoms will be diagnosed with SBS. In a typical clinical setting, cognitive biases that tend to lead to errors readily present themselves. These biases raise real questions about the rigor of “differential diagnosis,” the methodology that purports to rule out causes of the triad other than shaking. Overall, sustained examination of causation evidence, the rule in civil cases, has not penetrated criminal court, where judges are faced seemingly unawares with comparable admissibility decisions yet reflexively admit the proffered expert testimony. A look at SBS cases where missed diagnoses ultimately were identified shows that we cannot rely on our adversary system of justice to forestall the conviction of innocents.

The neurodegenerative dementias incorporate a range of pathological processes, many of which show distinctive clinical signatures. Although neurodegenerative processes are irreversible and difficult to modify pharmacologically, careful evaluation is an important part of the clinician's role, a major objective being to exclude alternative, potentially treatable causes of cognitive decline. The clinical categories that have emerged to classify the common causes of late-onset neurodegenerative dementia capture a range of clinically and pathologically distinct entities. Currently, however, the foremost practical consideration in the differential diagnosis of dementia is the need to identify those few cases in whom progressive cognitive dysfunction is a symptom of some more generalized (and possibly treatable) underlying condition, rather than secondary to a neurodegenerative process. This chapter, therefore, outlines a clinical approach to the cognitively impaired patient, aimed at distinguishing between these two broad groups.

This chapter examines the literature on children and adolescents with autism spectrum disorders in school-based settings. Reasons for the increasing prevalence rates are explored along with the challenges of differential diagnosis. The often unrecognized and undertreated mental health conditions that accompany autism spectrum disorders are discussed. The school mental health professional’s role in assessment and intervention is addressed, with attention paid to the use of response to intervention for children with autism spectrum disorders. The targeted classroom interventions of schedules, story-based interventions, modeling, and joint attention are reviewed. Opportunities to further support students with autism spectrum disorders are identified in collaboration with parents, teachers, and the community at large.

This chapter discusses psychogenic pruritus, which encompasses a heterogeneous group of diagnoses and is not just a diagnosis of exclusion. Psychogenic pruritus can be classified as pruritus precipitated and/or created by conscious behavioural response to underlying psychopathology and as pruritus initiated through unconscious pathological mental processing. The phenomenology and pathogenesis of psychogenic pruritus are discussed, and the authors also provide differential diagnosis for psychogenic pruritus. They furthermore consider whether psychogenic pruritus should stop during sleep or not, and study therapy and psychotropic drugs as ways to treat it.

The diagnosis of schizophrenia cannot be made based on the results of an ob­jective diagnostic test or laboratory measure, though we and others are working towards this. Instead, clinicians diagnose schizophrenia based on behaviour and psychopathology (including the symptoms described in the previous chapter). These require the subjective interpretation of clinicians, but they can be as­sessed reliably. The definitions of major mental illnesses used by clinicians are presented in the Diagnostic and Statistical Manual (DSM) of the American Psychiatric Association (in the United States) and the World Health Organization’s International Classification of Diseases (ICD) in other countries. These def­initions are updated from time to time to reflect gains in knowledge, or to reflect modern thinking on the similarities and differences between certain disorders. From one edition to the next, some diagnoses are revised, some are added, and some vanish altogether, only to be replaced or absorbed under other diagnoses. The diagnostic criteria for schizophrenia as defined by the most recent version of the DSM (DSM- 5) include the presence of two or more of the following symptoms: delusions, hallucinations, disorganized speech, disorganized or cata­tonic behaviour, and negative symptoms. At least one of the two must be delu­sions, hallucinations, or disorganized speech, while the second symptom type required for diagnosis could be any of the remaining four criteria. The require­ment of delusions, hallucinations, or disorganized speech maintains the resem­blance of the modern- day diagnosis to that first described by the clinician Emil Kraepelin over a century ago. Kraepelin’s discovery that schizophrenia is marked by a chronic and gradually worsening course is seen in modern- day criteria as well. A DSM-5 diagnosis of schizophrenia requires continuous signs of illness for at least 6 months, during which the individual must show at least 1 month of active symptoms (less if well treated). The diagnosis also requires social or work deterioration over a signifi­cant amount of time. Lastly, the diagnosis requires that the observed symptoms are not due to some other medical condition, including other psychiatric disorders such as bipolar disorder or major depressive disorder.

Positron emission tomography (PET) is a functional imaging technique utilized in Parkinson’s disease (PD) largely to assess the integrity of the nigrostriatal dopamine system. This chapter reviews the methodological aspects of dopaminergic PET imaging particularly involving specific radiotracer approaches to quantify pre- and postsynaptic function in health and disease. Also discussed are applications of dopaminergic PET for differential diagnosis, evaluation of non-motor disease manifestations, and the objective measurement of disease progression in clinical and genetic disease subtypes. The potential limitations of this imaging approach are also addressed.

Chapter 1 argues that careful diagnosis of injustices is central to understanding what to do about them. This requires differential diagnosis: the comparative assessment of different diagnoses of injustice. Yet present-day political theory treats such diagnostics as only a marginal task, even though past political theory considered it central. Chapter 1 undermines this marginalization, by tracing it to the tradition begun by John Rawls and its faulty practice of non-ideal theory. It argues that by the tradition’s own principles, non-ideal theory cannot succeed without such diagnostics. The chapter then recuperates such diagnostics by describing the leading theories of systematic injustice. These theories constitute the closest thing we have to a nosology (the classification of diseases) and pathology (the study of disease in general) of systematic injustice. If we wish to see political theory once again take seriously the differential diagnosis of injustices, then it will have to take these theories seriously.

As with all acute patients, always start by assessing ABCDE: airways, breathing, circulation, disability, and exposure. In a patient with acute gastrointestinal (GI) haemorrhage (whether upper or lower), assessing their circulation (i.e. haemodynamic status) is a priority. If there are clinical features to suggest haemodynamic instability—such as hypotension, tachycardia, cool peripheries, tachypnoea, or decreased consciousness—then the immediate priority is to resuscitate the patient before proceeding to a thorough history and examination. The differential diagnosis for rectal bleeding is shown in Figure 21.1. There are a couple of points to note about this differential diagnosis. GI haemorrhage may present as overt or occult bleeding. This table, and the indications of prevalence within it, refers to overt rectal bleeding as occult rectal bleeding will not be noticed by the patient. The second point to note is that upper GI sources of haemorrhage may occasionally present with rectal bleeding alone. Although it is more likely that such upper GI sources will also present with haematemesis, you should note that large volumes of blood in the GI tract can act as a cathartic (stimulant of peristalsis) and the resultant rapid transit through the intestine leads to the passage of red blood per rectum. • How much blood has been passed? This question is directly relevant to your initial haemodynamic status survey. Ask the patient to quantify approximately how much blood they have passed—familiar measures such as a teaspoon, eggcup, or wine glass may be easier for the patient than asking them to provide an estimate in millilitres. Note, however, that it is very easy to overestimate volumes of blood loss if, for example, blood has mixed with water in the toilet bowl. You should additionally enquire about symptoms of hypovolaemia—any light-headedness, collapse, chest pain or breathlessness? • What is the duration and frequency of the symptoms? • What did the blood look like? Generally speaking, the fresher the blood, the more distal the bleed. Substantial bleeding from lesions proximal in the GI tract may present with melaena (jet black, tarry stool caused by bacterial oxidation of haem) or may present as frank blood (haematochezia) if transit times are sufficiently rapid.

Attention deficit hyperactivity disorder (ADHD) is marked by problems with functioning or development that are related to symptoms of a persistent pattern of inattention and/or hyperactivity-impulsivity. It is the most common mental health problem in children, affecting as many as 1 in 20 children. It affects both boys and girls, but it is more predominant in boys. For males, prevalence rates are estimated to be three times that of females, 12.9% compared to 4.3%. Prevalence rates of ADHD in school-age children in the United States are estimated at 5% by the America Psychiatric Association. This chapter will focus on diagnosing and assessing ADHD from a differential diagnosis and comorbidity perspective. Evidenced-based ADHD interventions will be presented along with a discussion around the importance for school personnel to collaborate with the many other systems that impact children and youth with ADHD.

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) does not describe the typical symptoms noted by researchers of pediatric bipolar disorder under bipolar I or II because there is a great deal of controversy over whether bipolar disorder exists in children. Researchers who have gathered data on children who experience irritability, mood swings, elevated moods, inattention, hyperactivity, defiance, compulsive behaviors, sadness, and sleep problems have called the condition either pediatric bipolar disorder (PBD; for children 3–12) or early-onset bipolar disorder (EOBD; for children 13–18). Students with PBD or EOBD have little control over their mood swings and irritability, calling for a combination of pharmacological and environmental interventions along with close monitoring of any side effects and evaluation of the effectiveness of interventions. Bipolar disorder in children is considered a progressive condition that manifests differently as the child ages, moving from more irritability, restlessness, and rapid mood swings to less frequent mood swings but longer depressive moods.

This chapter examines John’s Medical Epitome. The focus here is on the first four of its six books. In contrast to the established view that this work was intended for physicians, it is argued that it was primarily written for philiatroi, intellectuals who were deeply interested in medicine, but not practising physicians themselves. The Medical Epitome, unlike John’s other two works, mainly consisted of material from earlier sources. The analysis of the text starts with a close reading of John’s proem and a discussion of the background of his dedicatee, the Byzantine statesman Alexios Apokaukos. It then shifts to an examination of the work’s structure with the aim of emphasizing John’s intentions in putting together his material. The analysis proceeds by way of a number of case studies focusing on diagnosis and therapy, and goes on to show that John intentionally condensed his material, removing specialized advice, so as to make it appeal to non-expert readers. Thus it is shown, for example, that the absence of details on invasive operations is consistent with the character of his intended readers, who were only able to use non-invasive techniques, such as phlebotomy and arteriotomy. Finally, the particular attention John paid to differential diagnosis, especially as regards eye affections, which is often supplemented with his own advice, is highlighted.

Sjögren’s is a complex disease that can manifest in a great variety of ways. Some patients may have dryness as the most prominent feature, while others can have life-threatening disease or considerable disability and involvement of multiple organs. The chameleonic nature of the disorder and the lack of a single diagnostic test often result in significant difficulty and delay in achieving a correct diagnosis. Even though Sjögren’s is present in many patients with autoimmune rheumatic disorders, the prominent manifestations of the disease are not always recognized. The resulting delay in diagnosis often is due to misinterpretation of clinical findings of synovitis, imaging abnormalities, and serology results, such as antinuclear antibodies and rheumatoid factor. This chapter discusses how practitioners can make a correct and reliable diagnosis that will result in optimal management for patients.

Chapter 6 presents case studies of diseases that afflict individuals rather than their communities at large. The conditions are presented in these categories: neoplastic diseases (cancers), congenital defects, infectious diseases, and diseases of unknown etiology. A differential diagnosis is made for each disease using a combination of the skeletal and medical evidence. The diseases are then discussed in terms of their likely impact on the lives of the afflicted individual.

The sinister causes can be remembered using the mnemonic VIVID: . . . Vascular: subarachnoid haemorrhage (SAH), haematoma (subdural or extradural), cerebral venous sinus thrombosis, cerebellar infarct Infection: meningitis, encephalitis Vision-threatening: temporal arteritis, acute glaucoma, cavernous sinus thrombosis, pituitary apoplexy, posterior leucoencephalopathy Intracranial pressure (raised): space-occupying lesion (SOL; e.g. tumour, abscess, cyst), cerebral oedema (e.g. trauma, altitude), hydrocephalus, malignant hypertension, idiopathic intracranial hypertension Dissection: carotid dissection . . . The approach to headache is the same as that to pain anywhere in the body: you need to start by characterizing the pain. One useful way of doing this is by following another mnemonic, SOCRATES: . . . Site of pain, and has it moved since it began? Onset of pain—was it sudden or gradual, and did something trigger it? Character of pain—throbbing, dull ache, sharp stabbing? Radiation of pain—has the pain spread? . . . Attenuating factors—does anything make the pain better (e.g. position, medications)? Timing of pain—how long has it gone on for, has it been constant or coming and going? Is it worse at a particular time of the day? Exacerbating factors—does anything make the pain worse (e.g. lying down, standing up, coughing, fatigue)? Severity—on a scale of 0 to 10, where 10 is the worst pain ever (e.g. childbirth). In addition, you should enquire about the presence or absence of the following ‘red flags’: • Decreased level of consciousness. This is a worrying feature of any medical presentation. Combined with headache, SAH needs exclusion. If there is a history of head injury, it could suggest a subdural haematoma (fluctuating consciousness) or extradural haematoma (altered consciousness following a lucid interval). Meningitis and encephalitis can also affect consciousness. • Sudden onset, worst headache ever. Suggests SAH, with blood in the cerebrospinal fluid (CSF) irritating the meninges. It can be informative to ask the patient whether they remember the exact moment when the headache started—a very severe headache of almost instantaneous onset is characteristic of SAH. Patients describe it like, for example, ‘being hit on the back of the head with a bat’.

Elimination disorders are sometimes considered the ugly step-child in psychiatry. Nocturnal enuresis is the voiding of urine at night and is always involuntary. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) specifically mentions antipsychotic medications as a potential cause. Encopresis is the repeated elimination of feces into inappropriate places, whether voluntary or involuntary. All children with elimination problems should see a pediatrician to rule out medical/physical causes. The prevalence of enuresis has been found to be higher in large or crowded families or in families that practice co-sleeping. A multitiered system of support approach begins with good toilet training and addresses occasional accidents. Simple behavioral treatments can usually resolve the problems. A case example illustrates a typical case.

Sjögren’s may occur in isolation or it may be found in association with another autoimmune disease. About half of those with Sjögren’s have Sjögren’s alone and about half have another major rheumatic, autoimmune disease with their Sjögren’s. Examples of autoimmune disorders associated with Sjögren’s include rheumatoid arthritis and systemic lupus erythematosus. Symptoms and signs caused by these associated autoimmune disorders can have an impact on treatment and potential complications in people with more than one related disease. Early and accurate diagnosis of associated autoimmune conditions is key to the successful management and long-term outcomes of Sjögren’s. The signs, symptoms, and relationship of these disorders to Sjögren’s are discussed in this chapter.