Deep brain stimulation is becoming very precise. This technique allows surgeons to place electrodes in almost any area of the brain.
over 6 years ago
Summary of these 3 key topics in psychiatry
over 9 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 8 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 11 years ago
Storylines on popular TV dramas are a great way of raising the public's awareness of a disease. They're almost as effective as a celebrity contracting an illness. For example, when Wiggles member Greg Page quit the group because of postural orthostatic tachycardia syndrome, I had a spate of patients, mostly young and female, coming in with self-diagnosed "Wiggles Disease". A 30% increase in the number of mammograms in the under-40s was attributed to Kylie Minogue's breast cancer diagnosis. The list goes on. Thanks to a storyline on the TV drama Desperate Housewives, I received questions about male postnatal depression from local housewives desperate for information: "Does it really exist?" "I thought postnatal depression was to do with hormones, so how can males get it?" "First it's male menopause, now it's male postnatal depression. Why can't they keep their grubby mitts off our conditions?" "It's like that politically correct crap about a 'couple' being pregnant. 'We' weren't pregnant, 'I' was. His contribution was five seconds of ecstasy and I was landed with nine months of morning sickness, tiredness, stretch marks and sore boobs!" One of my patients, a retired hospital matron now in her 90s, had quite a few words to say on the subject. "Male postnatal depression -- what rot! The women's liberation movement started insisting on equality and now the men are getting their revenge. You know, dear, it all began going downhill for women when they started letting fathers into the labour wards. How can a man look at his wife in the same way if he has seen a blood-and-muck-covered baby come out of her … you know? Men don't really want to be there. They just think they should -- it's a modern expectation. Poor things have no real choice." Before I had the chance to express my paucity of empathy she continued to pontificate. "Modern women just don't understand men. They are going about it the wrong way. Take young couples who live with each other out of wedlock and share all kind of intimacies. I'm not talking about sex; no, things more intimate than that, like bathroom activities, make-up removal, shaving, and so on." Her voice dropped to a horrified whisper. "And I'm told that some young women don't even shut the door when they're toileting. No wonder they can't get their de facto boyfriends to marry them. Foolish girls. Men need some mystery. Even when you're married, toileting should definitely be kept private." I have mixed feelings about male postnatal depression. I have no doubt that males can develop depression after the arrival of a newborn into the household; however, labelling it "postnatal depression" doesn't sit all that comfortably with me. I'm all for equality, but the simple fact of the matter is that males and females are biologically different, especially in the reproductive arena, and no amount of political correctness or male sharing-and-caring can alter that. Depressed fathers need to be identified, supported and treated, that goes without saying, but how about we leave the "postnatal" tag to the ladies? As one of my female patients said: "We are the ones who go through the 'natal'. When the boys start giving birth, then they can be prenatal, postnatal or any kind of natal they want!" (This blog post has been adapted from a column first published in Australian Doctor http://bit.ly/1aKdvMM)
Dr Genevieve Yates
over 8 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 8 years ago
A variety of psychological interventions to treat depressive disorders have been developed for use in primary care. Are some approaches more effective than others?
over 6 years ago
The Truth about Depression BBC Full Documentary 2013
about 7 years ago
If a pharmacologist has to name one of the finest medical marvels in the history of Neuro-pharmacology then Selective Serotonin Reuptake Inhibitors or SSRIs
almost 7 years ago
Identifying and Treating All Aspects of Fibromyalgia: A New Look Into a Painful Syndrome - Pain, Depression and Sleep
In this podcast, Drs. Andrew Cutler and Stephen M. Stahl discuss the myriad comorbidities associated with the syndrome of fibromyalgia. Patients often present complaining of fatigue as well as pain. Recent research suggests a link between pain, depression and sleep, which is discussed in this podcast.
Neuroscience Education Institute
over 11 years ago
Introduction Examination of the cranial nerves allows one to "view" the brainstem all the way from its rostral to caudal extent. The brainstem can be divided into three levels, the midbrain, the pons and the medulla. The cranial nerves for each of these are: 2 for the midbrain (CN 3 & 4), 4 for the pons (CN 5-8), and 4 for the medulla (CN 9-12). It is important to remember that cranial nerves never cross (except for one exception, the 4th CN) and clinical findings are always on the same side as the cranial nerve involved. Cranial nerve findings when combined with long tract findings (corticospinal and somatosensory) are powerful for localizing lesions in the brainstem. Cranial Nerve 1 Olfaction is the only sensory modality with direct access to cerebral cortex without going through the thalamus. The olfactory tracts project mainly to the uncus of the temporal lobes. Cranial Nerve 2 This cranial nerve has important localizing value because of its "x" axis course from the eye to the occipital cortex. The pattern of a visual field deficit indicates whether an anatomical lesion is pre- or postchiasmal, optic tract, optic radiation or calcarine cortex. Cranial Nerve 3 and 4 These cranial nerves give us a view of the midbrain. The 3rd nerve in particular can give important anatomical localization because it exits the midbrain just medial to the cerebral peduncle. The 3rd nerve controls eye adduction (medial rectus), elevation (superior rectus), depression (inferior rectus), elevation of the eyelid (levator palpebrae superioris), and parasympathetics for the pupil. The 4th CN supplies the superior oblique muscle, which is important to looking down and in (towards the midline). Pontine Level Cranial nerves 5, 6, 7, and 8 are located in the pons and give us a view of this level of the brainstem. Cranial Nerve 6 This cranial nerve innervates the lateral rectus for eye abduction. Remember that cranial nerves 3, 4 and 6 must work in concert for conjugate eye movements; if they don't then diplopia (double vision) results. The medial longitudinal fasciculus (MLF) connects the 6th nerve nucleus to the 3rd nerve nucleus for conjugate movement. Major Oculomotor Gaze Systems Eye movements are controlled by 4 major oculomotor gaze systems, which are tested for on the neurological exam. They are briefly outlined here: Saccadic (frontal gaze center to PPRF (paramedian pontine reticular formation) for rapid eye movements to bring new objects being viewed on to the fovea. Smooth Pursuit (parietal-occipital gaze center via cerebellar and vestibular pathways) for eye movements to keep a moving image centered on the fovea. Vestibulo-ocular (vestibular input) keeps image steady on fovea during head movements. Vergence (optic pathways to oculomotor nuclei) to keep image on fovea predominantly when the viewed object is moved near (near triad- convergence, accommodation and pupillary constriction) Cranial Nerve 5 The entry zone for this cranial nerve is at the mid pons with the motor and main sensory (discriminatory touch) nucleus located at the same level. The axons for the descending tract of the 5th nerve (pain and temperature) descend to the level of the upper cervical spinal cord before they synapse with neurons of the nucleus of the descending tract of the 5th nerve. Second order neurons then cross over and ascend to the VPM of the thalamus. Cranial Nerve 7 This cranial nerve has a motor component for muscles of facial expression (and, don't forget, the strapedius muscle which is important for the acoustic reflex), parasympathetics for tear and salivary glands, and sensory for taste (anterior two-thirds of the tongue). Central (upper motor neuron-UMN) versus Peripheral (lower motor neuron-LMN) 7th nerve weakness- with a peripheral 7th nerve lesion all of the muscles ipsilateral to the affected nerve will be weak whereas with a "central 7th ", only the muscles of the lower half of the face contralateral to the lesion will be weak because the portion of the 7th nerve nucleus that supplies the upper face receives bilateral corticobulbar (UMN) input. Cranial Nerve 8 This nerve is a sensory nerve with two divisions- acoustic and vestibular. The acoustic division is tested by checking auditory acuity and with the Rinne and Weber tests. The vestibular division of this nerve is important for balance. Clinically it be tested with the oculocephalic reflex (Doll's eye maneuver) and oculovestibular reflex (ice water calorics). Medullary Level Cranial nerves 9,10,11, and 12 are located in the medulla and have localizing value for lesions in this most caudal part of the brainstem. Cranial nerves 9 and 10 These two nerves are clinically lumped together. Motor wise, they innervate pharyngeal and laryngeal muscles. Their sensory component is sensation for the pharynx and taste for the posterior one-third of the tongue. Cranial Nerve 11 This nerve is a motor nerve for the sternocleidomastoid and trapezius muscles. The UMN control for the sternocleidomastoid (SCM) is an exception to the rule of the ipsilateral cerebral hemisphere controls the movement of the contralateral side of the body. Because of the crossing then recrossing of the corticobulbar tracts at the high cervical level, the ipsilateral cerebral hemisphere controls the ipsilateral SCM muscle. This makes sense as far as coordinating head movement with body movement if you think about it (remember that the SCM turns the head to the opposite side). So if I want to work with the left side of my body I would want to turn my head to the left so the right SCM would be activated. Cranial Nerve 12 The last of the cranial nerves, CN 12 supplies motor innervation for the tongue. Traps A 6th nerve palsy may be a "false localizing sign". The reason for this is that it has the longest intracranial route of the cranial nerves, therefore it is the most susceptible to pressure that can occur with any cause of increased intracranial pressure.
about 11 years ago
Previously I blogged about the 'stigma' and discrimination often faced by those confronting mental illness - even by colleagues. It was incredibly apt, therefore, that just a week later, the Royal College of Psychiatrists (RCPsych) published their "Parity" report. The report entitled Whole Person Care: from rhetoric to reality calls for an equality in physical vs mental health. As with many of my colleagues, I saw the word "Whole Person Care" and was instantly guilty of a pre-formed stereotype. I don't like the term whole person care nor holistic medicine. I hear these terms and my thoughts instantly switch to bright colours, 60s attire and I start humming "this is the dawning of the age of Aquarius". More so, this topic becomes riddled with questionable pseuodoscience and tentative nods to evidence-less forms of complimentary medicine. I think such terms are perhaps self destructive and instantly mark out mental health as odd. Ambiguous terms such as this make the whole topic even more off putting. Holistic rants aside, this report is an exceptionally important read (or at least glance) for all future doctors. There is an unquestionable inequality in mental and physical health in this country. It seems that if we can't 'see' something, it's not quantifiable and therefore loses a position of importance. It leads us to have 'pathological priorities', putting the physical before the mental. Despite this, both influence one another and deserve equal importance. Some of the key points of the report are: A call for equal funding of Mental and Physical Health Services A call to reduce discrimination and stigmas associated with Mental Health A call for equal care and treatment of Mental health/Physical Health A call for management and leaders (such as commissioning boards)to acknowledge the equality of mental/physical health Perhaps the most important for myself as I read through this was a call for equal access to Mental Health treatments under NICE clinical guidelines. Currently, patients have the right to receive only mental health treatments which have undergone NICE technology appraisals - not those offered by clinical guidelines. For example, NICE Clinical Guidelines state talk therapies are more effective than instant antidepressants for treatment of mild depression. The report is a huge step toward equality in mental and physical health. Perhaps we should all just take a moment to address the importance of both. You can read the full report and a summary on the RCPsych website here: http://www.rcpsych.ac.uk/usefulresources/publications/collegereports/op/op88.aspx
about 9 years ago
Black Box Warnings: Implications for Clinical Practice, Antidepressants, and Suicide, Part 3: Depression Treatment and Suicide Rates Following the Black Box Warnings
The podcast series titled "Black Box Warnings: Implications for Clinical Practice, Antidepressants, and Suicide" is divided into three parts. In Part 3, Drs. Sid Zisook and Stephen Stahl discuss an overview of the evidence regarding suicide and depression treatment trends since the implementation of the antidepressant black box warning, and guidance on appropriate monitoring strategies for patients with depression, with emphasis on the adolescent population.
Neuroscience Education Institute
over 11 years ago
Generalised Anxiety Disorder (GAD) Epidemiology Very common. Prevalence: Men – 2-4% Women 3-4.5% Accounts for 1/3 of all psychiatric diagnosis Accounts for 10% of all GP consultations Closely related to depression – and many patients move between the two states. Often patients satisfy the criteria for both anxiety and depression
almostadoctor.com - free medical student revision notes
about 8 years ago