Roger Seheult, MD illustrates the key differences between the nephrotic and nephritic syndromes. Topics include proteinuria, hematuria, casts, anatomy of the...
about 5 years ago
I started medical school in 2007 wanting to 'making people better'. I stopped medical school in 2010 facing the reality of not being able to get better myself, being ill and later to be diagnosed with several long term health conditions. This post is about my transition from being a medical student, to the other side - being a patient. There are many things I wish I knew about long-term health conditions and patients when I was a medical student. I hope that through this post, current medical students can become aware of some of theses things and put them into practice as doctors themselves. I went to medical school because I wanted to help people and make them better. I admired doctors up on their pedestals for their knowledge and skills and expertise to 'fix things'. The hardest thing for me was accepting that doctors can't always make people better - they couldn't make me better. Holding doctors so highly meant it was very difficult for me to accept their limitations when it came to incurable long-term conditions and then to accept that as a patient I had capacity myself to help my conditions and situation. Having studied medicine at a very academic university, I had a very strict perception of knowledge. Knowledge was hard and fast medical facts that were taught in a formal setting. I worked all day and night learning the anatomical names for all the muscles in the eye, the cranial nerves and citric acid cycle, not to mention the pharmacology in second year. Being immersed in that academic scientific environment, I correlated expertise with PhDs and papers. It was a real challenge to realise that knowledge doesn't always have to be acquired through a formal educational but that it can be acquired through experience. Importantly, knowledge acquired through experience is equally valid! This means the knowledge my clinicians have developed through studying and working is as valid as my knowledge of my conditions, symptoms and triggers, developed through experiencing it day in day out. I used to feel cross about 'expert patients' - I have spent all these hours in a library learning the biochemistry and pharmacology and 'Joe Bloggs' walks in and knows it all! That wasn't the right attitude, and wasn't fair on patients. As an expert patient myself now, I have come to understood that we are experts through different means, and in different fields. My clinicians remain experts in the biological aspects on disease, but that's not the full picture. I am an expert in the psychological and social impact of my conditions. All aspects need to be taken into account if I am going to have holistic integrated care - the biopsychosocial model in practice - and that's where shared-decision making comes in. The other concept which is has been shattered since making the transition from medical student to patient is that of routine. In my first rotation, orthopaedics and rheumatology, I lost track within the first week of how many outpatient appointments I sat in on. I didn't really think anything of them - they are just another 15 minute slot of time filled with learning in a very busy day. As a patient, my perspective couldn't be more different. I have one appointment with my consultant a year, and spend weeks planning and preparing, then a month recovering emotionally. Earlier this year I wrote a whole post just about this - The Anatomy of an Appointment. Appointments are routine for you - they are not for us! The concept of routine applies to symptoms too. After my first relapse, I had an emergency appointment with my consultant, and presented with very blurred vision and almost total loss of movement in my hands. That very fact I had requested an urgent appointment suggest how worried I was. My consultants response in the appointment was "there is nothing alarming about your symptoms". I fully appreciate that my symptoms may not have meant I was going to drop dead there and then, and that in comparison to his patients in ICU, I was not as serious. But loosing vision and all use of ones hands at the age of 23 (or any age for that matter) is alarming in my books! I guess he was trying to reassure me, but it didn't come across like that! I have a Chiari malformation (in addition to Postural Orthostatic Tachycardia Syndrome and Elhers-Danlos Syndrome) and have been referred to a neurosurgeon to discuss the possibility of neurosurgery. It is stating the obvious to say that for a neurosurgeon, brain surgery is routine - it's their job! For me, the prospect of even being referred to a neurosurgeon was terrifying, before I even got to the stage of discussing the operation. It is not a routine experience at all! At the moment, surgery is not needed (phew!) but the initial experience of this contact with neurosurgeons illustrates the concept of routines and how much our perspectives differ. As someone with three quite rare and complex conditions, I am invariable met in A&E with comments like "you are so interesting!". I remember sitting in the hospital cafeteria at lunch as a student and literally feasting on the 'fascinating' cases we had seen on upstairs on the wards that morning. "oh you must go and see that really interesting patient with X, Y and Z!" I am so thankful that you all find medicine so interesting - you need that passion and fascination to help you with the ongoing learning and drive to be a doctor. I found it fascinating too! But I no longer find neurology that interesting - it is too close to home. Nothing is "interesting" if you live with it day in day out. No matter what funky things my autonomic nervous may be doing, there is nothing interesting or fascinating about temporary paralysis, headaches and the day to day grind of my symptoms. This post was inspired by NHS Change Day (13th March 2013) - as a patient, I wanted to share these few things with medical students, what I wish I knew when I was where you are now, to help the next generation of doctors become the very best doctors they can. I wish you all the very best for the rest of your studies, and thank you very much for reading! Anya de Iongh www.thepatientpatient2011.blogspot.co.uk @anyadei
Anya de Iongh
about 7 years ago
In a recent article in the BMJ the author wonders about the reasons beyond the rising trend diagnosing Attention Deficit Hyperactivity Disorder (ADHD). The article attempts to infer reasons for this. One possible reason was that the diagnostic criteria especially DSM may seem for some to be more inclusive than ICD-10. The speculation may explain the rise of the diagnosis where DSM is used officially or have an influence. In a rather constructive way, an alternative to rushing to diagnosis is offered and discussed in some details. The tentative deduction that the Diagnostic Statistical Manual (DSM) may be one of the causes of rising diagnosis, due to raising the cut-off of age, and widening the inclusion criteria, as opposed to International Classification of Diseases, 10th revision (ICD-10), captured my attention. On reading the ICD-10 diagnostic criteria for research (DCR) and DSM-5 diagnostic criteria, I found them quite similar in most aspects, even the phraseology that starts with 'Often' in many diagnostic criteria, they seem to differ a bit in age. In a way both classification, are attempting to describe the disorder, however, it sounds as if someone is trying to explain a person's behaviour to you, however, this is not a substitute to direct clinical learning, and observing the behaviour, as if the missing sentence is 'when you see the person, it will be clearer'. El-Islam agrees with the notion that DSM-5 seems to be a bit more inclusive than ICD-10. A colleague of mine who is a child psychiatrist and she is doing her MSc. thesis in ADHD told me, that DSM-5 seems to be a substantial improvement as compared to its predecessor. The criteria - to her - though apparently are more inclusive, they are more descriptive with many examples, and she infers that this will payback in the reliability of the diagnosis. She hopes gene research can yield in biological tests for implicated genes and neurotransmitters in ADHD e.g. DRD4, DAT, gene 5,6,11 etc. One child psychiatrist, regretted the fact that misdiagnosis and under-diagnoses, deprive the patient from one of the most effective treatments in psychiatry. It is hoped the nearest forthcoming diagnostic classification (ICD-11), will address the issue of the diagnosis from a different perspective, or else converge with DSM-5 to provide coherence and a generalised newer standard of practice. The grading of ADHD into mild, moderate, and severe seem to blur the border between disorder and non-disorder, however, this quasi-dimensional approach seems realistic, it does not translate yet directly in differences in treatment approaches as with the case of mild, moderate, severe, and severe depression with psychotic symptoms, or intellectual disability. The author states that one counter argument could be that child psychiatrists are better at diagnosing the disorder. I wonder if this is a reflection of a rising trend of a disorder. If ADHD is compared to catatonia, it is generally agreed that catatonia is less diagnosed now, may be the epidemiology of ADHD is not artefact, and that we may need to look beyond the diagnosis to learn for example from environmental factors. Another issue is that there seems to be significant epidemiological differences in the rates of diagnosis across cultures. This may give rise to whether ADHD can be classified as a culture-bound syndrome, or whether it is influenced by culture like anorexia nervosa, or it may be just because of the raising awareness to such disorders. Historically, it is difficult to attempt to pinpoint what would be the closest predecessor to ADHD. For schizophrenia and mania, older terms may have included insanity, for depression it was probably melancholia, there are other terms that still reside in contemporary culture e.g. hypochondriasis, hysteria, paranoia etc. Though, it would be too simplistic to believe that what is meant by these terms was exactly what ancient cultures meant by them, but, they are not too far. ADHD seems to lack such historical underpinning. Crichton described a disorder he refers to as 'mental restlessness'. Still who is most often credited with the first description of ADHD, in his 1902 address to the Royal College of Physicians. Still describes a number of patients with problems in self-regulation or, as he then termed it, 'moral control' (De Zeeuw et al, 2011). The costs and the risks related to over-diagnosis, ring a warning bell, to enhance scrutiny in the diagnosis, due to subsequent stigma, costs, and lowered societal expectations. They all seem to stem from the consequences of the methodology of diagnosis. The article touches in an important part in the psychiatric diagnosis, and classifications, which is the subjective nature of disorders. The enormous effort done in DSM-5 & ICD-10 reflect the best available evidence, but in order to eliminate the subjective nature of illness, a biological test seems to be the only definitive answer, to ADHD in particular and psychiatry in general. Given that ADHD is an illness and that it is a homogeneous thing; developments in gene studies would seem to hold the key to understanding our current status of diagnosis. The suggested approach for using psychosocial interventions and then administering treatment after making sure that it is a must, seems quite reasonable. El-Islam, agrees that in ADHD caution prior to giving treatment is a recommended course of action. Another consultant child psychiatrist mentioned that one hour might not be enough to reach a comfortable diagnosis of ADHD. It may take up to 90 minutes, to become confident in a clinical diagnosis, in addition to commonly used rating scales. Though on the other hand, families and carers may hypothetically raise the issue of time urgency due to scholastic pressure. In a discussion with Dr Hend Badawy, a colleague child psychiatrist; she stated the following with regards to her own experience, and her opinion about the article. The following is written with her consent. 'ADHD is a clinically based diagnosis that has three core symptoms, inattention, hyperactivity and impulsivity in - at least - two settings. The risk of over-diagnosis in ADHD is one of the potentially problematic, however, the risk of over-diagnosis is not confined to ADHD, it can be present in other psychiatric diagnoses, as they rely on subjective experience of the patient and doctor's interviewing skills. In ADHD in particular the risk of under-diagnosis is even more problematic. An undiagnosed child who has ADHD may suffer various complications as moral stigma of 'lack of conduct' due to impuslivity and hyperactivity, poor scholastic achievement, potential alienation, ostracization and even exclusion by peer due to perceived 'difference', consequent feelings of low self esteem and potential revengeful attitude on the side of the child. An end result, would be development of substance use disorders, or involvement in dissocial behaviours. The answer to the problem of over-diagnosis/under-diagnosis can be helped by an initial step of raising public awareness of people about ADHD, including campaigns to families, carers, teachers and general practitioners. These campaigns would help people identify children with possible ADHD. The only risk is that child psychiatrists may be met with children who their parents believe they might have the disorder while they do not. In a way, raising awareness can serve as a sensitive laboratory investigation. The next step is that the child psychiatrist should scrutinise children carefully. The risk of over-diagnosis can be limited via routine using of checklists, to make sure that the practice is standardised and that every child was diagnosed properly according to the diagnostic criteria. The use of proper scales as Strengths and Difficulties Questionnaire (SDQ) in its two forms (for parents SDQ-P and for teachers SDQ-T) which enables the assessor to learn about the behaviour of the child in two different settings. Conner's scale can help give better understanding of the magnitude of the problem. Though some people may voice criticism as they are mainly filled out by parents and teachers, they are the best tools available at hands. Training on diagnosis, regular auditing and restricting doctors to a standard practice of ensuring that the child and carer have been interviewed thoroughly can help minimise the risk of over-diagnosis. The issue does not stop by diagnosis, follow-up can give a clue whether the child is improving on the management plan or not. The effects and side effects of treatments as methylphenidate should be monitored regularly, including regular measurement height and weight, paying attention to nausea, poor appetite, and even the rare side effects which are usually missed. More restrictions and supervision on the medication may have an indirect effect on enhancing the diagnostic assessment. To summarise, the public advocacy does not increase the risk of over-diagnosis, as asking about suicidal ideas does not increase its risk. The awareness may help people learn more and empower them and will lead to more acceptance of the diagnosed child in the community. Even the potential risk of having more case loads for doctors to assess for ADHD may help give more exposure of cases, and reaching more meaningful epidemiological finding. From my experience, it is quite unlikely to have marked over-representation of children who the families suspect ADHD without sufficient evidence. ADHD remains a clinical diagnosis, and it is unlikely that it will be replaced by a biological marker or an imaging test in the near future. After all, even if there will be objective diagnostic tests, without clinical diagnostic interviewing their value will be doubtful. It is ironic that the two most effective treatments in psychiatry methylphenidate and Electroconvulsive Therapy (ECT) are the two most controversial treatments. May be because both were used prior to having a full understanding of their mechanism of action, may be because, on the outset both seem unusual, electricity through the head, and a stimulant for hyperactive children. Authored by E. Sidhom, H. Badawy DISCLAIMER The original post is on The BMJ doc2doc website at http://doc2doc.bmj.com/blogs/clinicalblog/#plckblogpage=BlogPost&plckpostid=Blog%3A15d27772-5908-4452-9411-8eef67833d66Post%3Acb6e5828-8280-4989-9128-d41789ed76ee BMJ Article: (http://www.bmj.com/content/347/bmj.f6172). Bibliography Badawy, H., personal communication, 2013 El-Islam, M.F., personal communication, 2013 Thomas R, Mitchell GK, B.L., Attention-deficit/hyperactivity disorder: are we helping or harming?, British Medical Journal, 2013, Vol. 5(347) De Zeeuw P., Mandl R.C.W., Hulshoff-Pol H.E., et al., Decreased frontostriatal microstructural organization in ADHD. Human Brain Mapping. DOI: 10.1002/hbm.21335, 2011) Diagnostic Statistical Manual 5, American Psychiatric Association, 2013 Diagnostic Statistical Manual-IV, American Psychiatric Association, 1994 International Classification of Diseases, World Health Organization, 1992
Dr Emad Sidhom
over 6 years ago
Mitral valve prolapse(MVP) (a.k.a. floppy mitral valve syndrome, systolic click murmur syndrome or billowing mitral leaflet) is a valvular heart disease characterized by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole. It is the primary form of myxomatous degeneration of the valve. There are various types of MVP, broadly classified as classic and nonclassic. In its nonclassic form, MVP carries a low risk of complications and often can be kept minimal by dietary attention. In severe cases of classic MVP, complications include mitral regurgitation, infective endocarditis, congestive heart failure, and, in rare circumstances, cardiac arrest.
over 4 years ago
Metabolic syndrome and obesity are attaining epidemic proportions worldwide. This PPT shows the link between the two, their aetiology, the pathophysiology and what simple measures could be used in managing the conditions.
over 7 years ago
Cranial Nerve 1- Olfaction This patient has difficulty identifying the smells presented. Loss of smell is anosmia. The most common cause is a cold (as in this patient) or nasal allergies. Other causes include trauma or a meningioma affecting the olfactory tracts. Anosmia is also seen in Kallman syndrome because of agenesis of the olfactory bulbs. Cranial Nerve 2- Visual acuity This patientâs visual acuity is being tested with a Rosenbaum chart. First the left eye is tested, then the right eye. He is tested with his glasses on so this represents corrected visual acuity. He has 20/70 vision in the left eye and 20/40 in the right. His decreased visual acuity is from optic nerve damage. Cranial Nerve II- Visual field The patient's visual fields are being tested with gross confrontation. A right sided visual field deficit for both eyes is shown. This is a right hemianopia from a lesion behind the optic chiasm involving the left optic tract, radiation or striate cortex. Cranial Nerve II- Fundoscopy The first photograph is of a fundus showing papilledema. The findings of papilledema include 1. Loss of venous pulsation 2. Swelling of the optic nerve head so there is loss of the disc margin 3. Venous engorgement 4. Disc hyperemi 5. Loss of the physiologic cup an 6. Flame shaped hemorrhages. This photograph shows all the signs except the hemorrhages and loss of venous pulsations. The second photograph shows optic atrophy, which is pallor of the optic disc resulting form damage to the optic nerve from pressure, ischemia, or demyelination. Images Courtesy Dr. Kathleen Digre, University of Uta Cranial Nerves 2 & 3- Pupillary Light Refle The swinging flashlight test is used to show a relative afferent pupillary defect or a Marcus Gunn pupil of the left eye. The left eye has perceived less light stimulus (a defect in the sensory or afferent pathway) then the opposite eye so the pupil dilates with the same light stimulus that caused constriction when the normal eye was stimulated. Video Courtesy of Dr.Daniel Jacobson, Marshfield Clini and Dr. Kathleen Digre, University of Uta Cranial Nerves 3, 4 & 6- Inspection & Ocular Alignmen This patient with ocular myasthenia gravis has bilateral ptosis, left greater than right. There is also ocular misalignment because of weakness of the eye muscles especially of the left eye. Note the reflection of the light source doesn't fall on the same location of each eyeball. Video Courtesy of Dr.Daniel Jacobson, Marshfield Clini and Dr. Kathleen Digre, University of Uta Cranial Nerves 3, 4 & 6- Versions • The first patient shown has incomplete abduction of her left eye from a 6th nerve palsy. • The second patient has a left 3rd nerve palsy resulting in ptosis, dilated pupil, limited adduction, elevation, and depression of the left eye. Second Video Courtesy of Dr.Daniel Jacobson, Marshfield Clini and Dr. Kathleen Digre, University of Uta Cranial Nerves 3, 4 & 6- Duction Each eye is examined with the other covered (this is called ductions). The patient is unable to adduct either the left or the right eye. If you watch closely you can see nystagmus upon abduction of each eye. When both eyes are tested together (testing versions) you can see the bilateral adduction defect with nystagmus of the abducting eye. This is bilateral internuclear ophthalmoplegia often caused by a demyelinating lesion effecting the MLF bilaterally. The adduction defect occurs because there is disruption of the MLF (internuclear) connections between the abducens nucleus and the lower motor neurons in the oculomotor nucleus that innervate the medial rectus muscle. Saccades Smooth Pursui The patient shown has progressive supranuclear palsy. As part of this disease there is disruption of fixation by square wave jerks and impairment of smooth pursuit movements. Saccadic eye movements are also impaired. Although not shown in this video, vertical saccadic eye movements are usually the initial deficit in this disorder. Video Courtesy of Dr.Daniel Jacobson, Marshfield Clini and Dr. Kathleen Digre, University of Utah Optokinetic Nystagmu This patient has poor optokinetic nystagmus when the tape is moved to the right or left. The patient lacks the input from the parietal-occipital gaze centers to initiate smooth pursuit movements therefore her visual tracking of the objects on the tape is inconsistent and erratic. Patients who have a lesion of the parietal-occipital gaze center will have absent optokinetic nystagmus when the tape is moved toward the side of the lesion. Vestibulo-ocular refle The vestibulo-ocular reflex should be present in a comatose patient with intact brainstem function. This is called intact "Doll’s eyes" because in the old fashion dolls the eyes were weighted with lead so when the head was turned one way the eyes turned in the opposite direction. Absent "Doll’s eyes" or vestibulo-ocular reflex indicates brainstem dysfunction at the midbrain-pontine level. Vergenc Light-near dissociation occurs when the pupils don't react to light but constrict with convergence as part of the near reflex. This is what happens in the Argyll-Robertson pupil (usually seen with neurosyphilis) where there is a pretectal lesion affecting the retinomesencephalic afferents controlling the light reflex but sparing the occipitomesencephalic pathways for the near reflex. Video Courtesy of Dr.Daniel Jacobson, Marshfield Clini and Dr. Kathleen Digre, University of Uta Cranial Nerve 5- Sensor There is a sensory deficit for both light touch and pain on the left side of the face for all divisions of the 5th nerve. Note that the deficit is first recognized just to the left of the midline and not exactly at the midline. Patients with psychogenic sensory loss often identify the sensory change as beginning right at the midline. Cranial Nerves 5 & 7 - Corneal refle A patient with an absent corneal reflex either has a CN 5 sensory deficit or a CN 7 motor deficit. The corneal reflex is particularly helpful in assessing brainstem function in the unconscious patient. An absent corneal reflex in this setting would indicate brainstem dysfunction. Cranial Nerve 5- Motor • The first patient shown has weakness of the pterygoids and the jaw deviates towards the side of the weakness. • The second patient shown has a positive jaw jerk which indicates an upper motor lesion affecting the 5th cranial nerve. First Video Courtesy of Alejandro Stern, Stern Foundation Cranial Nerve 7- Motor • The first patient has weakness of all the muscles of facial expression on the right side of the face indicating a lesion of the facial nucleus or the peripheral 7th nerve. • The second patient has weakness of the lower half of his left face including the orbicularis oculi muscle but sparing the forehead. This is consistent with a central 7th or upper motor neuron lesion. Video Courtesy of Alejandro Stern, Stern Foundatio Cranial Nerve 7- Sensory, Tast The patient has difficulty correctly identifying taste on the right side of the tongue indicating a lesion of the sensory limb of the 7th nerve. Cranial Nerve 8- Auditory Acuity, Weber & Rinne Test This patient has decreased hearing acuity of the right ear. The Weber test lateralizes to the right ear and bone conduction is greater than air conduction on the right. He has a conductive hearing loss. Cranial Nerve 8- Vestibula Patients with vestibular disease typically complain of vertigo – the illusion of a spinning movement. Nystagmus is the principle finding in vestibular disease. It is horizontal and torsional with the slow phase of the nystagmus toward the abnormal side in peripheral vestibular nerve disease. Visual fixation can suppress the nystagmus. In central causes of vertigo (located in the brainstem) the nystagmus can be horizontal, upbeat, downbeat, or torsional and is not suppressed by visual fixation. Cranial Nerve 9 & 10- Moto When the patient says "ah" there is excessive nasal air escape. The palate elevates more on the left side and the uvula deviates toward the left side because the right side is weak. This patient has a deficit of the right 9th & 10th cranial nerves. Video Courtesy of Alejandro Stern, Stern Foundatio Cranial Nerve 9 & 10- Sensory and Motor: Gag Refle Using a tongue blade, the left side of the patient's palate is touched which results in a gag reflex with the left side of the palate elevating more then the right and the uvula deviating to the left consistent with a right CN 9 & 10 deficit. Video Courtesy of Alejandro Stern, Stern Foundation Cranial Nerve 11- Moto When the patient contracts the muscles of the neck the left sternocleidomastoid muscle is easily seen but the right is absent. Looking at the back of the patient, the left trapezius muscle is outlined and present but the right is atrophic and hard to identify. These findings indicate a lesion of the right 11th cranial nerve. Video Courtesy of Alejandro Stern, Stern Foundation Cranial Nerve 12- Moto Notice the atrophy and fasciculation of the right side of this patient's tongue. The tongue deviates to the right as well because of weakness of the right intrinsic tongue muscles. These findings are present because of a lesion of the right 12th cranial nerve.
about 9 years ago
In the initial interviews with patients who suffer psychotic symptoms, it might be striking that the usage of terminology of descriptive psychopathology lingers on an arbitration of knowledge of 'truth' by using terms like delusions or hallucinations with their definition as false beliefs or false perceptions (Casey & Kelly 2007). These terms can cause annihilation of value to patient's experience, which may pose an initial strain on the egalitarian patient-doctor relationship. In an era, where deference to experts is dead, it might be worthy on agreeing on the effect of these experiences prior to lablelling them. Delusions can not be objectively detected and described, because it evolves and exists within subjective and interpersonal dimensions. Severe psycopathological symptoms share the fact that they are statistically deviant, and thus can be labeled as 'unshared'. Symptoms may be perceived as 'distressing' and they might be 'disabling' to them. The outcome behaviour which may raise concern can be a 'dysfunctional' behaviour (Adams & Sutker 2004). Jaspers considered the lack of understandability of how the patient reached conclusion to be the defining factor of a delusional idea. The notion of defining 'delusion' as false belief was challenged by Jaspers. Sims gives the example of a man who believed his wife was unfaithful to him because the fifth lamp-post alone on the left was unlit. What makes it a delusion is the methodology not the conclusion which may be right (Sims 1991). Some delusions might be mundane in their content, others may not be falsifiable. Dereistic thinking is not based on logic but rather on feelings. It is possible to find ways to evade falsification; an ad hoc hypotheses may also be part of the presentation. Fish stated that delusional elaboration may follow delusion and/or hallucination which may have convergence with the concept of the ad hoc hypothesis. Absence of verification from the patient's side does not lead to deductive falsification (Casey & Kelly 2007). Otherwise, the doctor-patient relationship carry the risk to transform to detective-suspect relationship, where the latter may perceive the need to present evidence of innocence. Mental health professionals are usually encountered by people who suffer to various degrees or make others suffer, and not because of various degrees of conviction. The primary role of the therapist is to be defined as some one who tries to alleviate the sufferings of others rather than correcting their beliefs. Communicating with patients in terms of how functional is their belief rather than it's truth may prove to be more egalitarian and clinically tuned. This may provide some middle ground in communication, without having to put an effort on defining the differences between what is 'true' and what is 'real'. The criterion for demarcation between what is real and what is pathologic may be different in the patient-doctor relationship. The assertion on the clinician's part on the falsity of a belief or experience can have the risk of dogmatism. The statistical deviance of symptoms, their distressing nature, disabling consequences, the resultant dysfunctional behaviour and apparent leap from evidence to conclusion may be a more agreeable surrogate starting points. This might be more in line with essence of medicine or 'ars medicina' (art of healing). Concordance with patients on their suffering may serve as an egalitarian platform prior to naming the symptoms. The term delusion commonly identified as false fixed belief, when used by a psychiatrist, it does not address only a symptom. It rather puts the interviewer in the position of an all knowing judge. After all, a service-user may argue that how come a doctor who never encountered or experienced any of the service-user's aspects of the problem as being persecuted at work and home, as plainly false. Then, does the psychiatrist know the truth. From a service-user point of view what he/she experience is real; which might not necessarily be true. The same applies for people who lead an average life, people who go to work bearing with them their superstitions, beliefs about ghosts, luck, horoscopes, zodiacs, or various revered beliefs. This term has the risk of creating a temporary crack in the mutual sense of equality between the therapist and the service-user. This may be due to the labelling of certain dysfunctional belief as unreal by one side. It has the potential for a subtle change in the relationship to the mental health professional placing himself/herself in the omniscient position and it contrasts with the essence of medical practice where practitioners assume the truth in what the patients say as in the rest of subjective symptoms as headache for example. The subsequent sequel of this is other labels such as 'bizarre delusions' or 'systematised delusions', further add to the deviation of the role of the professional therapist to an investigator in the domain of 'Truth' and architecture of 'Truth'. Furthermore, it might be strenuous to the relationship when the therapist - based on skeptic enquiry - starts explaining such symptoms. For example, if the service-user believes that Martians have abducted him, implanted a device in his brain and sent him/her back to earth, and the response communicated back is the 'delusional'. It could be argued by the service-user that the therapist who had not seen a Martian or a brain device before, labelled the whole story as 'delusion' in a rather perceived dismissive labelling with no intention to check on the existence of Martians or the device. In other words, the healer became the arbiter of truth, where both lack evidence for or against the whole thing; one member in the relationship stepped into power on basis of subjective view of plausibility or lack of thereof. In the case of hallucinations, the clinician labelling the patient's experience as hallucinations can be imposing fundamental dilemma for the patient. For example, if a patient hears a voice that says that everything is unreal apart from the voice, and the clinician says that the voice is the thing that is unreal. Both do not give evidence to their 'truth' apart from their statement. The clinician's existence to the patient's subjective reality is distorted by the multiple realities of the patient, and arguing on basis of mere existence that the 'voice' is the one that is 'false', does not give the patient a clue of the future methodology to discern from both, since percetption is deceived and/or distorted. In this case, another tool of the mind can be employed to address the patient. The same can be applied to a concept like 'over valued ideas', where the clinician decides that this particular idea is 'over valued', or that this 'idea' is 'over valued' in a pathological way. The value put on these ideas or not the patient values but the clinician's evaulation of 'value' and 'pathology'. The cut of point of 'value' and 'over value' seems to be subjective from the clinician's perspective. Also, 'derailment' pauses the notion of expecting a certain direction of talk. The concepts of 'grooming' and 'eye contact' implicitly entail the reference to a socio-cultural normative values. Thus, deviation from the normative value is reflected to the patient as pathology, which is an ambiguous definition, in comparison to the clarity of pathology. The usage of terms like 'dysfunctional unshared belief' or 'distressing auditory perception' or other related terms that address the secondary effect of a pathologic experience may be helpful to engage with the patient, and may be more logically plausible and philosophically coherent yet require empirical validation of beneficence. Taylor and Vaidya mention that it is often helpful to normalise, but this is not to minimise or be dismissive of patient's delusional beliefs.(Taylor & Vaidya 2009). The concept can be extended to cover other terms such as 'autistic thinking, 'apathy', 'blunting of affect', 'poor grooming', 'over-valued ideas', other terms can be applied to communicate these terms with service-users with minimal deviation from the therapeutic relationship. The limitation of these terms in communication of psychopathology are special circumstances as folie a deux, where a dysfunctional belief seems to be shared with others Also, symptoms such as Charles-Bonnet syndrome; usually does not have negative consequences. The proposed terms are not intended for use as a replacement to well carved descriptive psychopathological terms. Terms like 'delusion' or 'hallucination' are of value in teaching psychopathology. However in practice, meaningful egalitarian communication may require some skill in selecting suitable terms that is more than simplifying jargon. They also may carry the burden of having to add to the psychiatric terminology with subsequent effort in learning them. They can also be viewed as 'euphemism' or 'tautology'. However, this has been the case from 'hysteria' to 'medically unexplained symptoms' which seems to match with the zeitgeist of an era where 'Evidence Based Medicine' is its mantra; regardless advances in treatment. Accuracy of terminology might be necessary to match with essence of scientific enquiry; systematic observation and accurate taxonomy. The author does not expect that such proposal would be an easy answer to difficulties in communication during practice. This article may open a discussion on the most effective and appropriate terms that can be used while communicating with patients. Also, it might be more in-line with an egalitarian approach to seek to the opinion of service-users and professional bodies that represent the opinions of service-users. Empirical validation and subjection of the concept to testing is necessary. Patient's care should not be based on logic alone but rather on evidence. Despite the limitations of such proposal with regards to completeness, it's hoped that the introduction of any term may help to add to the main purpose of any classification or labelling that is accurate egalitarian communication. DISCLAIMER This blog is adapted from BMJ doc2doc clinical blogs Philosophical Streamlining of Psychopathology and its Clinical Implications http://doc2doc.bmj.com/blogs/clinicalblog/_philosophical-streamlining-of-psychopathology-its-clinical-implications The blog is based on an article named 'Towards a More Egalitarian Approach to Communicating Psychopathology' which is published in the Journal of Ethics in Mental Health, 2013 http://www.jemh.ca/issues/v8/documents/JEMHVol8Insight_TowardsaMoreEgalitarianApproachtoCommunicatingPsychopathology.pdf Bibliography Adams, H. E., Sutker P.B. (2004). Comprehensive Handbook of Psychopathology. New York: Springer Science Casey, P., Kelly B., (2007). Fish's Clinical Psychopathology: Signs and Symptoms in Psychiatry, Glasgow: Bell & Bain Limited Kingdon and Turkington (2002), The case study guide to congitive behavior therapy for psychosis, Wiley Kiran C. and Chaudhury S. (2009). Understanding delusion, Indian Journal of Psychiatry Maddux and Winstead (2005). Psychopathology foundations for a contemporary understanding, Lawrence Erlbaum Associates Inc. Popper (2005) The logic of scientific discovery, Routledge, United Kingdom Sidhom, E. (2013) Towards a More Egalitarian Approach to Communicating Psychopathology, JEMH · 2013· 8 | 1 © 2013 Journal of Ethics in Mental Health (ISSN: 1916-2405) Sims A., Symptoms in the mind, (1991) an introduction to psychopathology, Baillere Tindall Taylor and Vaidya (2009), Descriptive psychopathology, the signs and symptoms of behavioral disorders, Cambridge university press
Dr Emad Sidhom
over 6 years ago
Through different periods of the Egyptian history from Pharaonic, Greco-Roman, Coptic, Islamic and Modern Era; Egyptians tend to respect, appreciate and care for elderly. There is also a rich Eastern Christian tradition in respecting and taking care of old people that has continued since the first centuries of Christianity. Churches used to develop retirement homes served by monastic personnel and nurses. Egyptian culture traditionally linked some aspects of mental illnesses to sin, possession of evil, separation from the divine and it is usually associated with stigmatisation for all family members. However, forgetfulness with ageing was normalised. Until now, it seems that the difference between normal ageing and dementia is blurred for some people. Recently, the term 'Alzheimer' became popular, and some people use it as synonymous to forgetfulness. El-Islam, stated that some people erroneously pronounce it as 'Zeheimer' removing the 'Al' assuming it is the Arabic equivalent to the English 'the'. In 2010, a film was produced with the title 'Zeheimer' confirming the mispronunciation. Elderly face many health challenges which affect their quality of life. Dementia is one of these challenges as it is considered to be one of the disorders which attack elderly and affect their memory, mental abilities, independence, decision making and most cognitive functions. Therefore, the focus on dementia has increased around the world due to the rapid spread of the syndrome and the economical and psychosocial burden it cause for patients, families and communities. (Grossber and Kamat 2011, Alzheimer’s Association 2009, Woods et al. 2009). In recent years, the proportion of older people is increasing due to the improvement in health care and scientific development. The demographic transition with ageing of the population is a global phenomenon which may demand international, national, regional and local action. In Egypt the ageing population at the age of 65 and older are less than 5% of the Egyptian population (The World FactBook, 2012), yet, the World Health Organization (WHO) asserts that a demographic shift is going to happen as most of the rapid ageing population will transfer to the low and middle income countries in the near future (WHO, 2012). Egyptian statistics assert this shift. The Information Decision Support Center published the first comprehensive study of the elderly in Egypt in 2008. According to the report, in 1986, 5 percent of Egyptians were age 60 and older. In 2015, they will make up to 11 percent of the population and in 2050; over a fifth. Caring of older persons constitutes an increasing segment of the Egyptian labor market. However, nation wide statistics about number of dementia sufferers in Egypt may be unavailable but the previous demographic transition is expected to be accompanied by an increase in dementia patients in Egypt and will affect priorities of health care needs as well. The Egyptian society may need adequate preparation with regards to health insurance, accommodation and care homes for the upcoming ageing population (El-Katatney, 2009). Although the number of care home increased from 29 in 1986 to be around 140 home in 2009; it cannot serve more than 4000 elderly from a total of 5 million. Not every elderly will need a care home but the total numbers of homes around Egypt are serving less than 1% of the elderly population. These facts created a new situation of needs for care homes besides the older people who are requiring non-hospital health care facility for assisted living. The Egyptian traditions used to be strongly associated with the culture of extended family and caring for elderly as a family responsibility. Yet, in recent years changes of the economic conditions and factors as internal and external immigration may have affected negatively on elderly care within family boundaries. There is still the stigma of sending elderly to care homes. Some perceive it as a sign of intolerance of siblings towards their elderly parents but it is generally more accepted nowadays. Therefore, the need for care homes become a demand at this time in Egypt as a replacement of the traditional extended family when many older people nowadays either do not have the choice or the facilities to continue living with their families (El-Katatney 2009). Many families among the Egyptian society seem to have turned from holding back from the idea of transferring to a care home to gradual acceptance since elderly care homes are becoming more accepted than the past and constitutes a new concept of elderly care. Currently, many are thinking to run away from a lonely empty home in search of human company or respite care but numbers of geriatric homes are extremely lower than required and much more are still needed (Abdennour, 2010). Thus, it seems that more care homes may be needed in Egypt. Dementia patients are usually over 65, this is one of the factors that put them at high risk of exposure to different physical conditions related to frailty, old age, and altered cognitive functions. Additionally, around 50% of people with dementia suffers from other comorbidities which affect their health and increases hospital admissions (National Audit Office 2007). Therefore, it is expected that the possibility of doctors and nurses needing to provide care for dementia patients in various care settings is increasing (RCN 2010). Considering previous facts, we have an urgent need in Egypt to start awareness about normal and upnormal ageing and what is the meaning of dementia. Moreover, change of health policies and development of health services is required to be developed to match community needs. Another challenge is the very low number of psychiatric doctors and facilities since the current state of mental health can summarised as; one psychiatrist for every 67000 citizens and one psychiatric hospital bed for every 7000 citizens (Okasha, 2001). Finally the need to develop gerontologically informed assessment tools for dementia screening to be applied particularly in general hospitals (Armstrong and Mitchell 2008) would be very helpful for detecting dementia patients and develop better communication and planning of care for elderly. References: El Katateny, E. 2009. Same old, same old: In 2050, a fifth of Egyptians will be age 60 and older. How will the country accommodate its aging population?. Online available at: http://etharelkatatney.wordpress.com/category/egypt-today/page/3/ Fakhr-El Islam, M. 2008. Arab culture and mental health care. Transcultural Psychiatry, vol. 45, pp. 671-682 Ageing and care of the elderly. Conference of European churches. 2007. [online] available at: http://csc.ceceurope.org/fileadmin/filer/csc/Ethics_Biotechnology/AgeingandCareElderly.pdf World Health Organization. 2012 a. Ageing and life course: ageing Publications. [Online] available at : http://www.who.int/ageing/publications/en/ World Health Organization. 2012 b. Ageing and life course: interesting facts about ageing. [Online] available at: http://www.who.int/ageing/about/facts/en/index.html World Health Organization 2012 c. Dementia a public health priority. [online] available at: http://whqlibdoc.who.int/publications/2012/9789241564458_eng.pdf World Health Organization. 2012 d. Why focus on ageing and health, now?. Department of Health. 2009. Living well with dementia: a national dementia strategy. [Online] available at: http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_094058 Andrawes, G., O’Brien, L. and Wilkes, L. 2007. Mental illness and Egyptian families. International Journal of Mental Health Nursing, vol.16, pp. 178-187 National Audit Office. 2007. Improving service and support for people with dementia. London. [online[ Available at: http://www.nao.org.uk/publications/0607/support_for_people_with_dement.aspx Armstrong, J and Mitchell, E. 2008. Comprehensive nursing assessment in the care of older people. Nursing Older People, vol. 20, No. 1, pp. 36-40. Okasha, A. 2001. Egyptian contribution to the concept of mental health. Eastern Mediterranean Health Journal,Vol. 7, no. 3, pp. 377-380. Woods, R., Bruce, E., Edwards, R., Hounsome, B., Keady, J., Moniz-Cook, E., Orrell, M. and Tussell, I. 2009. Reminiscence groups for people with dementia and their family carers: pragmatic eight-centre randomised trial of joint reminiscence and maintenance versus usual treatment: a protocol. Trials Journal: open access, Vol. 10, [online] available at: http://www.trialsjournal.com/content/10/1/64 Grossberg, G. and Kamat, S. 2011. Alzheimer’s: the latest assessment and treatment strategies. Jones and Bartlett, publisher: The United States of America. Alzheimer’s Association. 2009. 2009 Alzheimer’s disease facts and figures. Alzheimer’s & Dementia, Volume 5, Issue 3. [online] Available at: http://www.alz.org/news_and_events_2009_facts_figures.asp Royal College of Nursing. 2010. Improving quality of care for people with dementia in general hospitals. London. National Audit Office. 2007. Improving service and support for people with dementia. London. [online[ Available at: http://www.nao.org.uk/publications/0607/support_for_people_with_dement.aspx Authors: Miss Amira El Baqary, Nursing Clinical instructor, The British University in Egypt email@example.com Dr Emad Sidhom, MBBCh, ABPsych-Specialist in Old Age Psychiatry-Behman Hospital firstname.lastname@example.org
Amira El Baqary
about 6 years ago
“Spinal cord syndromes? I love those, and never forget them!” – Said nobody, ever. Despite the fact that spinal cord syndromes can be difficult to remember, they are important to recognize and can yield a significant amount of clinical information. We seek to break spinal cord syndromes into an easy to digest and understand discussion.
over 4 years ago
It’s quick, it’s easy and we’ve all done it. Don’t blush, whether it’s at our leisure or behind the consultant’s back we can confess to having used the world’s sixth most popular website. You might have seen it, sitting pride of place on the podium of practically any Google result page. Of course, it’s the tell tale sign of one of Web 2.0’s speediest and most successful offspring, Wikipedia. Now for fear of patronizing a generation who have sucked on the teat of this resource since its fledgling years, the formalities will remain delightfully short. Wikipedia is the free, multilingual, online encyclopedia, which harnesses the collective intelligence of the world’s internet users to produce a collaboratively written and openly modifiable body of knowledge. The technology it runs on is a highly flexible web application called wiki. It is open-source software; hence the explosion of wiki sites all united under the banner of combined authorship. Anyone with internet access can edit the content and do so with relative anonymity. It would be unthinkable that a source, which does not prioritize the fidelity of its content, could possibly play a role in medical education. How ironic it seems that medical students can waste hours pondering which textbook to swear their allegiance for the forthcoming rotation, yet not spare a second thought typing their next medical query into Wikipedia. Evidently it has carved itself a niche and not just among medical students, but healthcare professionals as well. According to a small qualitative study published in the International Journal of Medical Informatics, 70% of their sample, which comprised of graduates from London medical schools currently at FY2 and ST1 level, used Wikipedia in a given week for ‘clinical purposes’. These ranged from general background reading to double checking a differential and looking up medications. We are so ensnared by the allure of instantaneous enlightenment; it’s somewhat comparable to relieving an itch. "Just Google it..." is common parlance. We need that quick fix. When the consultant asks about his or her favourite eponymous syndrome or you’re a little short on ammunition before a tutorial, the breadth and ease-of-use offered by a service accessible from our phones is a clandestine escape. The concept of Wikipedia, the idea that its articles are in a way living bodies because of the continual editing process, is its strength. Conversely textbooks are to a degree outmoded by the time they reach their publication date. While I commend the contributors of Wikipedia for at least trying to bolster their pages with references to high impact journals, it does not soften the fact that the authorship is unverifiable. Visitors, lay people, registered members under some less than flattering pseudonyms such as Epicgenius and Mean as custard, don’t impart the sense of credibility students (or for that matter patients)expect from an encyclopedia. Since the prestige of direct authorship if off the cards, it does beg the question of what is their motivation and I’m afraid ‘the pursuit of knowledge and improving humanity’s lot' is the quaint response. There is a distinct lack of transparency. It has become a playground where a contributor can impress his/her particular theory regarding a controversial subject unchallenged. Considering there is no direct ownership of the article, who then has the authority to curate the multiple theories on offer and portray a balanced view? Does an edit war ensue? It is not unheard of for drug representatives to tailor articles detailing their product and erase the less pleasant side-effects. Obviously Wikipedia is not unguarded, defences are in place and there is such a thing as quality control. Recent changes will come under the scrutiny of more established editors, pages that are particularly prone to vandalism are vetted and there are a special breed of editors called administrators, who uphold a custodial post, blocking and banishing rebellious editors. A study featured in the First Monday journal put Wikipedia to the test by deliberately slipping minor errors into the entries of past philosophers. Within 48 hours half of these errors had been addressed. Evidently, the service has the potential to improve over time; provided there is a pool of committed and qualified editors. Wikiproject Medicine is such a group of trusted editors composed primarily of doctors, medical students, nurses, clinical scientists and patients. Since 2004, its two hundred or so participants have graded an excess of 25,000 health-related articles according to quality parameters not dissimilar to peer review. However, the vast majority of articles are in a state of intermediate quality, somewhere between a stub and featured article. Having some degree of professional input towards a service as far reaching as Wikipedia will no doubt have an impact on global health, particularly in developing countries where internet access is considered a luxury. March this year saw the medical pages of the English Wikipedia reach a lofty 249,386,264 hits. Its ubiquity is enviable; it maintains a commanding lead over competing medical websites. The accessibility of this information has catapulted Wikipedia far beyond its scope as a humble encyclopedia and into a medical resource. Patients arrive to clinics armed with the printouts. As future doctors we will have to be just that one step ahead, to recognise the limitations of a source that does not put a premium on provenance but is nevertheless the current public health tool of choice. Illustrator Edward Wong This blog post is a reproduction of an article published in the Medical Student Newspaper, November 2013 issue.
about 6 years ago
In NeuroPsychiatry it might be difficult to locate its territory, and find its niche. This might be an uneasy endeavour as its two parent branches neurology and psychiatry are still viable, also it siblings organic psychiatry, behavioural neurology and biological psychiatry are also present. This blogpost attempts to search for the definition and domains of neuropsychiatry. Neuropsychiatry can be defined as the 'biologic face' of mental health (Royal Melbourne Hospital, Neuropsychiatry unit). It is the neurological aspects of psychiatry and the psychiatric aspects of neurology (Pacific Neurpsychiatry Institute). It is not a new term. Many physicians used to brand themselves as neuropsychiatrists at the rise of the twentieth century. It has been looked upon with a sense of unease as a hybrid branch. Also, it was subject to pejorative connotations, as the provenance of amateurs in both parent disciplines (Lishman, 1987). The foundational claim is that 'all' mental disorders are disorders of the brain' (Berrios and Marková, 2002). The American NeuroPsychiatric Association (ANPA) defines it as 'the integrated study of psychiatric and neurologic disorders' (ANPA, 2013). The overlap between neuropsychiatry and biological psychiatry was observed (Trimble and George, 2010) as the domain of enquiry of the first and the approach of the second will meet at point. Berrios and Marková seemed to have focused on the degree of conversion among biological psychiatry, organic psychiatry, neuropsychiatry and behavioural neurology. They stated that they share the same foundational claims (FCcs): (1) mental disorder is a disorder of the brain; (2) reasons are not good enough as causes of mental disorder; and (3) biological psychiatry and its congeners have the patrimony of scientific truth. They further elaborated that the difference is primarily due to difference in historic origins. (D'haenen et al., 2002). The American Neuropsychiatric Association (ANPA) defines neuropsychiatry as the integrative study of neurological and psychiatric disorders on a clinical level, on a theoretical level; ANPA defines it as the bridge between neuroscience and clinical practice. The interrelation between both specialities is adopted by The Royal Australia and New Zealand College of Psychiatrists as it defines it as a psychiatric subspeciality. This seems to resonate the concept that 'biologisation' of psychiatry is inevitable (Sachdev and Mohan, 2013). The definition according to Gale Encyclopedia encompasses the interface between the two disciplines (Fundukian and Wilson, 2008). In order to acknowledge the wide use of the term 'neuropsychiatry'; the fourth edition of Lishman's Organic Psychiatry, appeared and it was renamed as 'textbook of neuropsychiatry'. The editor stated that the term is not used in its more restrictive sense (David, 2009). Ostow backtracked the origin of biological causes for illness to humoral view of temperament.In the nineteenth century, the differentiation between both did not seem to be apparent. The schism seems to have emerged in the twentieth century. The difficulties that arose with such early adoption of neuronal basis to psychiatric disorders are that they were based on on unsubstantiated beliefs and wild logic rather than scientific substance. (Panksepp, 2004). Folstein stated that Freud and Charcot postulated psychological and social roots for abnormal behaviours, thus differentiating neurology from psychiatry. (David, 2009). The separation may have lead to alienation of doctors on both camps and helped in creating an arbitary division in their scope of knowledge and skills. The re-emergence of interest in neurospsychiatry has been described to be due to the growing sense of discomfort in the lack of acknowledgment of brain disorders when considering psychiatric symptoms (Arciniegas and Beresford, 2001). There is considerable blurring regarding defining the territory and the boundaries of neuropsychiatry. The Royal College of Psychiatrists founded section of Neuropsychiatry in 2008. The major working groups include epilepsy, sleep disorders, brain injury and complex neurodisability. In 1987 the British NeuroPsychiatry Association was established, to address the professional need for distinction, without adopting the concept of formal affiliation with parent disciplinary bodies as the Royal College of Psychiatrists. The ANPA was founded in 1988. It issued training guide for residents. The guide included neurological and psychiatric assessments, interpretation of EEG and brain imaging techniques. With regards to the territory, it included delirium, dementia, psychosis, mood and anxiety disorders due to general medical condition. Neurpsychiatric aspects of psychopharmacologic treatments, epilepsy, neuropsychiatric aspects of traumatic brain injury and stroke. The diagnosis of movement disorders, neurobehavioural disorders, demyelinating disease, intellectual and developmental disorders, as well as sleep disorders was also included. The World Federation of Societies of Biological Psychiatry (WFSBP) was established in Buenos Aires in 1974 to address the rising significance of biological psychiatry and to join local national societies together. The National Institute of Mental Health (NIMH), is currently working on a biologically-based diagnosis, that incorporates neural circuits, cells, molecules to behavioural changes. The diagnostic system - named 'Research Domain Criteria (RDoC) - is agnostic to current classification systems DSM-5 & ICD-10. Especially that the current diagnostic classficiations are mostly based on descriptive rather than neurobiological aetiological basis. (Insel et al., 2010). For example, the ICD-10 F-Code designates the first block to Organic illness, however, it seems to stop short of localisation of the cause of illness apart from the common prefix organic. It also addresses adverse drug events as tardive dyskinesia but stops short of describing it neural correlates. Also, psychosocial roots of mental illness seem to be apparent in aetiologically-based diagnoses as Post-Traumatic Stress Disorder, acute stress reaction, and adjustment disorders, the diagnostic cluster emphasise the necessity of having 'stress'. Other diagnoses seem to draw from the psychodynamic literature, e.g. conversion[dissociative] disorder. The need for neuropsychiatry, has been increasing as the advances in diagnostic imaging and laboratory investigations became more clinically relevant. Nowadays, there are tests as DaT-Scan that can tell the difference between neurocognitive disorder with Lewy Bodies and Parkinson's Disease. Vascular neurocognitive disorders warrant imaging as the rule rather than the exception, vascular depression has been addressed is a separate entity. Frontal Lobe Syndromes have been subdivided into orbitofrontal and dorsolateral (Moore,2008) Much training is needed to address this subspeciality. The early cases that may have stirred up the neurological roots of psychiatric disorders can be backdated to the case of Phineas Gage, and later, the case H.M. The eearlier fruits of adopting a neuropsychiatric perspective can be shown in the writings of Eliot Slater, as he attempted to search for the scientific underpinnings of psychiatry, and helped via seminal articles to highlight the organic aspect of psychiatry. Articles like 'The diagnosis of "Hysteria", where Slater, challenged the common wisdom of concepts like hysteria and conversion, rejecting the social roots of mental illness, and presenting a very strong case for the possibility of organicity, and actual cases of for which 'hysteria' was a plain misdiagnosis was way ahead of its time prior to CT Brain. Slater even challenged the mere existence of the concept of 'hysteria. (Slater, 1965) Within the same decade Alwyn Lishman published his textbook 'Organic Psychiatry' addressing the organic aspects of psychiatric disorders. Around the same time, the pioneers of social/psychological roots of mental illness became under attack. Hans Eysenck, published his book 'Decline and Fall of the Freudian Empire'. Eysenck stated clearly that the case of Anna O. seems to have been mispresented and that she never had 'hysteria' and recovered she actually had 'tuberculous meningitis' and she died of its complications (Eysenck, 1986). To summarise, it seems difficult and may be futile to sharply delineate neurpsychiatry, biological psychiatry, organic psychiatry and behavioural neurology. However, it seems important to learn about the biological psychiatry as an approach and practice neuropsychiatry as a subspeciality. The territory is yet unclear from gross organic lesions as stroke to the potential of encompassing entire psychiatry as the arbitary distinction between 'functional' and 'organic' fades away. Perhaps practice will help to shape the domain of the speciality, and imaging will guide it. To date, the number of post-graduate studies are still low in comparison to the need for such speciality, much more board certification may be needed as well as the currently emerging masters and doctoral degrees. This post is previously posted on bmj doc2doc blogs Bibliography Eysenck, H.J., Decline and Fall of the Freudian Empire, Pelican Series, 1986 German E Berrios, I.S.M., The concept of neuropsychiatry: A historical overview, Journal of Psychosomatic Research, 2002, Vol. 53, pp. 629-638 Kieran O’Driscoll, J.P.L., “No longer Gage”: an iron bar through the head, British Medical Journal, 1998, Vol. 317, pp. 1637-1638 Perminder S. Sachdev, A.M., Neuropsychiatry: Where Are We And Where Do We Go From Here?, Mens Sana Monographs, 2013, Vol. 11(1), pp. 4-15 Slater, E., The Diagnosis of "Hysteria", British Medical Journal, 1965, Vol. 5447(1), pp. 1395–1399 Thomas Insel, Bruce Cuthbert, R.H.M.G.K.Q.C.S.P.W., Research Domain Criteria (RDoC): Toward a New Classification Framework for Research on Mental Disorders, American Journal of Psychiatry, 2010, Vol. 167:7, pp. 748-751 Organic Psychiatry, Anthony S. David, Simon Fleminger, M. D. K. S. L. J. D. M. (ed.), Wiley-Blackwell, 2009 Neuropsychiatry an introductory approach, Arciniegas & Beresford (ed.), Cambridge University Press, 2001 Biological Psychiatry, Hugo D’haenen, J.A. den Boer, P. W. (ed.), John Wiley and Sons, 2010 Gale Encyclopedia of Mental Health, Laurie J. Fundukian, J. W. (ed.), Thomson Gale, 2008 Biological Psychiatry, M. Trimble, M. G. (ed.), Wiley-Blackwell, 2010 Textbook of Neuropsychiatry, Moore, D. P. (ed.), Hodder Arnold, 2008 Textbook of Biological Psychiatry, Panksepp, J. (ed.), John Wiley and Sons, 2004 The American Neuropsychiatric Association Website www.anpaonline.org The Royal Melbourne Neuropsychiatry Unit Website http://www.neuropsychiatry.org.au/ The British Neuropsychiatry Association website www.bnpa.org.uk The Royal College of Psychiatrists website www.rcpsych.ac.uk The World Federation of Societies of Biological Psychiatry website www.wfsbp.org
Dr Emad Sidhom
almost 6 years ago
This month’s case is by David R Bell PhD, co-author of Medical Physiology: Principles for Clinical Medicine, 3e (ISBN: 9781451110395) For more information, or to purchase your copy, visit: http://tiny.cc/Rhoades4e, with 15% off using the discount code: MEDUCATION. The case below is followed by a quiz question, allowing you a choice of diagnoses. Select the one letter section that best describes the patient’s condition. The Case A 28-year old woman has an unremarkable pregnancy through her first 28 weeks of gestation, with normal weight gain and no serious complications. She has no previous history of diabetes, hypertension of other systemic disease before or during her current pregnancy. During her 30-week checkup, her blood pressure measures 128/85, and she complains about feeling slightly more “bloated” than usual with swelling in her legs that seems to get more uncomfortable as the day goes on. Her obsterician recommends that she get more bed rest, stay off her feet as much as possible and return for evaluation in one week. At the one-week follow-up, the patient presents with noticable”puffiness” in her face, and a blood pressure of 145/95. She complains she has been developing headaches, sporadic blurred vision, right-sided discomfort and some shortness of breath. She has gained more than 10 lb (4.5kg) in the past week. A urinalysis on the patient revelas no glucose but a 3+ reading for protein. Her obstetrician decides to admit her immediately to a local tertiary care hospital for further evaluation. Over the next 24 hours, the patient’s urine output is recorded as 500mL and contains 6.8 grams of protein. Her plasma albumin level is 3.1 g/dl, hemacrit 48%, indirect bilirubin 1.5mg/dl and blood platelets=77000/uL, respectively. Her blood pressure is now 190/100. It is decided to try to deliver the foetus. The expelled placenta is small and shows signs of widespread ischmic damage. Within a week of delivery, the mother’s blood pressure returns to normal, and her oedema subsides. One month later, the mother shows no ill effects of thos later-term syndrome. Question What is the clinical diagnosis of this patient’s condition and its underlying pathophysiology? A. Gestational Hypertension B. Preeclampsia C. Gestational Diabetes D. Compression of the Inferior Vena Cava Answer The correct answer is "B. Preeclampsia". The patient’s symptoms and laboratory findings are consistent with a diagnosis of Preeclampsia, which is a condition occurring in some pregnancies that causes life-threatening organ and whole body regulatory malfunctions. The patient’s negative urine glucose is inconsistent with gestational diabetes. Gestational hypertension or vena caval compression cannot explain all of the patient findings. The patient has three major abnormal findings- generalised oedema, hypertension and proteinuria which are all common in preeclampsia. Although sequalae of a normal pregnancy can include water and salt retention, bloating, modest hypertension and leg swelling (secondary to capillary fluid loss from increased lower limb capillary hydrostatic pressure due to compression of the inferior vena cava by the growing foetus/uterus), oedema in the head and upper extremities, a rapid 10 pound weight gain and shortness of breath suggests a generalized and serious oedematous state. The patient did not have hypertension before or within 20 weeks gestation (primary hypertension) and did not develop hypertension after the 20th week of pregnancy with no other abnormal findings (gestational hypertension). Hypertension with proteinuria occurring beyond the 20th week of pregnancy however is a hallmark of preeclampsia. In addition, the patient has hemolysis (elevated bilirubin and LDH levels), elevated liver enzyme levels and thrombocytopenia. This is called the HELLP syndrome (HELLP = Hemolysis, Elevated Liver enzymes and Low Platelets.), and is considered evidence of serious patient deterioration in preeclampsia. A urine output of 500 ml in 24 hours is 1/2 to 1/4 of normal output in a hydrated female and indicates renal insufficiency. Protein should never be found in the urine and indicates loss of capillaries integrity in glomeruli which normally are not permeable to proteins. The patient has substantial 24 urine protein loss and hypoalbuminemia. However, generally plasma albumin levels must drop below 2.5 gm/dl to decrease plasma oncotic pressure enough to cause general oedema. The patient’s total urinary protein loss was insufficient in this regard. Capillary hyperpermeability occurs with preeclampsia and, along with hypertension, could facilitate capillary water efflux and generalized oedema. However myogenic constriction of pre-capillary arterioles could reduce the effect of high blood pressure on capillary water efflux. An early increase in hematocrit in this patient suggests hemoconcentration which could be caused by capillary fluid loss but the patient’s value of 48 is unremarkable and of little diagnostic value because increased hematocrit occurs in both preeclampsia and normal pregnancy. PGI2, PGE2 and NO, produced during normal pregnancy, cause vasorelaxation and luminal expansion of uterine arteries, which supports placental blood flow and development. Current theory suggests that over production of endothelin, thromboxane and oxygen radicals in preeclampsia antagonize vasorelaxation while stimulating platelet aggregation, microthrombi formation and endothelial destruction. These could cause oedema, hypertension, renal/hepatic deterioration and placental ischemia with release of vasotoxic factors. The patient’s right-sided pain is consistent with liver pathology (secondary to hepatic DIC or oedematous distention). Severe hypertension in preeclampsia can lead to maternal end organ damage, stroke, and death. Oedematous distension of the liver can cause hepatic rupture and internal hemorrhagic shock. Having this patient carry the baby to term markedly risks the life of the mother and is not considered current acceptable clinical practice. Delivery of the foetus and termination of the pregnancy is the only certain way to end preeclampsia. Read more This case is by David R Bell PhD, co-author of Medical Physiology: Principles for Clinical Medicine, 3e (ISBN: 9781451110395) For more information, or to purchase your copy, visit: http://tiny.cc/Rhoades4e. Save 15% (and get free P&P) on this, and a whole host of other LWW titles at (lww.co.uk)[http://lww.co.uk] when you use the code MEDUCATION when you check out! About LWW/ Wolters Kluwer Health Lippincott Williams and Wilkins (LWW) is a leading publisher of high-quality content for students and practitioners in medical and related fields. Their text and review products, eBooks, mobile apps and online solutions support students, educators, and instiutions throughout the professional’s career. LWW are proud to partner with Meducation.
Lippincott Williams & Wilkins
about 7 years ago
It was a Saturday, about tea-time in the quaint village of Athelstaneford, East Lothian. Mrs Alexandria Agutter sat in her cottage, enjoying the delights of the late-summer evening with a glass of gin and tonic. She listlessly sipped from the rather generous pick-me up, no doubt chewing over the happenings of the day. Blast! The taste was much too bitter to her liking. She stood up. And promptly crumpled to the floor in a dizzied heap. It had not been five minutes when a fiery pain gripped her parched throat and in her frenzied turn she watched the bleary room become draped in a gossamery silk. How Dame Agatha would approve. But this is no crime novel, on that fateful day, 24th August 1994, poor Mrs Agutter immortalised herself in the history books of forensic medicine; she was the victim of a revered toxin and a vintage one it was too. She had unwittingly imbibed a G&T laced with a classic poison of antiquity. A clue from the 21st century: do you recall the first Hunger Games film adaption? Those inviting purple-black berries or as Suzanne Collins coined them ‘Nightlock’; a portmanteau of hemlock and Deadly Nightshade. True to the laters’ real life appearance those onscreen fictional fruits played a recurring cameo role. Deadly Nightshade is a perennial shrub of the family Solanaceae and a relative of the humble potato (a member of the Solanus genus). It is a resident of our native woodland and may be found as far afield as Europe, Africa and Western Asia. The 18th century taxonomist, Carl Linnaeus gave the plant an intriguing name in his great Species Plantarum. The genus Atropa is aptly named after one of the three Greek Fates, Atropos. She is portrayed shearing the thread of a mortal’s life so determining the time and manner of its inevitable end. The Italian species name belladona (beautiful woman) refers to the striking mydriatic effect of the plant on the eye. The name pays homage to Pietro Andre Mattioli, a 16th century physician from Sienna, who was allegedly the first to describe the plant’s use among the Venetian glitterati - ladies of fashion favoured the seductive, doe-eyed look. Belladona is poisonous in its entirety. It was from the plant’s roots in 1831, the German apothecary Heinrich F. G. Mein isolated a white, odourless, crystalline powder: it was (surprise, surprise) atropine. Atropine is a chiral molecule. From its natural plant source it exists as a single stereoisomer L-atropine, which also happens to display a chiral potency 50-100 times that of its D-enantiomer. As with many other anaesthetic agents it is administered as a racemic mixture. How strange that atropine now sits among the anaesthetist’s armamentarium, its action as a competitive antimuscarinic to counter vagal stimulation belies its dark history. It was a favourite of Roman housewives seeking retribution against their less than faithful husbands and a staple of the witch’s potion cupboard. Little wonder how belladona became known as the Devil’s plant. Curiouser still it’s also the antidote for other poisons, most notably the organophosphates or nerve gases. On account of its non-selective antagonism, atropine produces a constellation of effects: the inhibition of salivary, lacrimal and sweat glands occurs at low doses; dry mouth and skin are early markers. Pyrexia is a central effect exacerbated by the inability to sweat. Flushing of the face due to skin vessel vasodilatation. Low parasympathetic tone causes a moderate sinus tachycardia. Vision is blurred as the eye becomes dilated, unresponsive to light and accommodation is impaired. Mental disorientation, agitation and ataxia give the impression of drunkedness or a delirium tremens like syndrome. Visual hallucinations, often of butterflies or silk blowing in the wind, are a late feature. It was then that Mr Agutter, seemingly untroubled by the sight of his wife’s problematic situation, proceeded to leave a message with the local practitioner. How fortunate they were to have the vigilant locum check the answering machine and come round to the Agutter’s lodge accompanied by an ambulance crew. The attending paramedic had the presence of mind to pour the remainder of Mrs Agutter’s beverage into a nearby jam jar, while Mr Agutter handed over what he suspected to be the offending ingredient: the bottle of Indian tonic water. As it soon transpired there were seven other casualties in the surrounding countryside of East Lothian – all involving an encounter with tonic water. In fact by some ironic twist of fate, two of the victims were the wife and son of Dr Geoffry Sharwood-Smith, a consultant aneasthetist. Obviously very familiar with the typical toxidrome of anticholinergic agents, he was quick to suspect atropine poisoning. Although for a man of his position with daily access to a sweetshop of drugs, it was not something to draw attention to. Through no small amount of cunning had the poisoner(s) devised the plan. It was elegant; atropine is very bitter. So much so that it can be detected at concentrations of 100 parts per million (0.001%). Those foolish enough to try the berries of belladonna during walks in the woods are often saved by the berry’s sour taste. They are soon spat out. But the quinine in the tonic water was a worthy disguise. The lethal dose for an adult is approximately 90-130mg, however atropine sensitivity is highy variable. In its salt form, atropine sulfate, it is many times more soluble: >100g can be dissolved in 100ml of water. So 1ml may contain roughly tenfold the lethal dose. There ensued a nationwide scare; 50 000 bottles of Safeway branded Indian tonic water were sacrificed. Only six bottles had been contaminated. They had all been purchased, tops unsealed, from the local Safeway in Hunter’s Tryst. Superficially this looked like the handiwork of a psychopath with a certain distaste for the supermarket brand, and amidst the media furore, it did have some verisimilitude: one of the local papers received a letter from 25 year old, Wayne Smith admitting himself as the sole perpetrator. The forensic scientist, Dr Howard Oakley analysed the contents of the bottles. They all contained a non-lethal dose, 11-74mg/litre of atropine except for the Agutter’s, it contained 103mg/litre. The jam jar holding Mrs Agutter’s drink bore even more sinister results, the atropine concentration was 292mg/L. It would appear Mrs Agutter had in some way outstayed her welcome. But she lived. A miscalculation on the part of the person who had added an extra seasoning of atropine to her drink. According to the numbers she would have had to swallow a can’s worth (330ml) to reach the lethal dose. Thankfully she had taken no more than 50mg. The spotlight suddenly fell on Dr Paul Agutter. He was a lecturer of biochemistry at the nearby University of Napier, which housed a research syndicate specialising in toxicology. CCTV footage had revealed his presence at the Safeway in Hunter’s Tryst and there was eye witness evidence of him having placed bottles onto the shelves. Atropine was also detected by the forensic investigators on a cassete case in his car. Within a matter of two weeks he would be arrested for the attempted murder of his wife. Despite the calculated scheme to delay emergency services and to pass the blame onto a non-existent mass poisoner, he had not accomplished the perfect murder. Was there a motive? Allegedly his best laid plans were for the sake of a mistress, a mature student from Napier. He served seven years of a twelve year sentence. Astonishingly, upon his release from Glenochil prison in 2002, he contacted his then former wife proclaiming his innocence and desire to rejoin her in their Scottish home. A proposition she was not very keen on. Dr Agutter was employed by Manchester University as a lecturer of philosophy and medical ethics. He is currently an associate editor of the online journal Theoretical Biology and Medical Modelling. We will never know the true modus operandi as Dr Agutter never confessed to the crime. Perhaps all this story can afford is weak recompense for the brave followers of the Dry January Campaign. Oddly these sort of incidents never appear in their motivational testimonials. Acknowledgements Emsley J. Molecules of Murder. 2008, Cambridge, RSC Publishing, p.46-67. Lee MR. Solanaceae IV: Atropa belladona, deadly nightshade. J R Coll Physicians Edinb. March 2007; 37: 77-84. Illustrator Edward Wong This blog post is a reproduction of an article published in the The Medical Student Newspaper January issue, 2014 http://www.themedicalstudent.co.uk/
over 6 years ago
Kanner’s infantile autism and Asperger’s syndrome -- Pearce 76 (2): 205 -- Journal of Neurology, Neurosurgery & Psychiatry
Recent much publicised attention to autism and its putative relation to the measles, mumps, and rubella (MMR) vaccination reminds us that autism affects approximately 4 in 10 000 of the population. It is characterised by impairments in reciprocal social interaction and communication, restricted and stereotyped patterns of interests and activities, and the presence of developmental abnormalities by 3 years of age. Much of the psychiatric literature appears to overlook the organic basis,1 with subtle neurological signs evident in many examples: learning difficulties, a high incidence of epilepsy, viral infections, tuberous sclerosis, and fragile X syndrome are known associations.
almost 5 years ago