Pupillary Unrest Correlates with Arousal Symptoms and Motor Signs

Total Page:16

File Type:pdf, Size:1020Kb

Pupillary Unrest Correlates with Arousal Symptoms and Motor Signs BRIEF REPORTS Decades of Delayed Diagnosis We report 4 patients with young-onset parkinson- ism, each of whom was misdiagnosed with a motor in 4 Levodopa-Responsive conversion disorder for at least a decade after their Young-Onset Monogenetic first specialist referral. Parkinsonism Patients Case reports Patient 1 Helen Ling, BScMed, BMBS, MSc,1,2 Mark Braschinsky, A British woman developed gait freezing at age 31 3 3 3 MD, PhD, Pille Taba, MD, Siiri-Merike Lu¨ u¨ s, MD, Karen during her first pregnancy. She then became unsteady Doherty, MB, BCh, BAO, MRCP,1,2 Anna Hotter, MD,4 4 1,2 and clumsy and complained of jerky tremulous hands Werner Poewe, MD, and Andrew J. Lees, MD FRCP * and curling of the toes. She also complained of pro- found fatigue and slowness of thinking. At age 37, she 1Reta Lila Weston Institute of Neurological Studies, Institute of Neurology, University College London, London, United Kingdom; started to have urinary urgency and to fall over. Over 2Queen Square Brain Bank for Neurological Disorders and Institute 14 years, she was seen by 6 neurologists and had of Neurology, University College London, London, United Kingdom; received diagnoses of motor conversion disorder 3Department of Neurology, University of Tartu, Tartu, Estonia; (MCD), chronic fatigue syndrome (CFS), and depres- 4 Department of Neurology, University Hospital of Innsbruck, Austria sion. Her movements were described as distractible, variable, and deliberately slow. Her spontaneous move- ments were considered as strikingly normal in contrast with those found on formal neurological examination. At age 45, she was reviewed at the National Hospital for Neurology and Neurosurgery in Queen Square, ABSTRACT London, where Parkinson’s disease was suspected. Background: We report 4 patients with young-onset In 2001, her brother committed suicide, which coin- monogenetic parkinsonism, each of whom was misdiag- cided with a marked deterioration in her physical symp- nosed with either a psychogenic movement disorder or chronic fatigue syndrome for 10 to 23 years after the toms at age 37. Three of her other 5 siblings had received onset of their first symptoms. psychiatric treatment for depression. Her mother had a Results: Once the diagnosis was eventually made, they longstanding history of severe depression. all had a rapid and excellent response to levodopa, albeit On examination, she walked with 2 sticks and a nar- with the early appearance of interdose dyskinesias in 3. row-based gait with stooped posture and postural insta- Conclusions: We discuss possible reasons for the bility (Video 1a). She had a melancholic, slightly anxious missed diagnosis despite the relentless progression facial expression, an asymmetrical fast resting tremor of their motor handicap. DAT scanning supported the that was also present on posture and action, and a fast revised clinical diagnosis of parkinsonism. VC 2011 Movement Disorder Society synchronous rest tremor in both legs. Her movements were very slow. Finger tapping revealed progressive Key Words: parkin; monogenetic parkinsonism; psy- reduction in amplitude without motor arrests or fatigue. chogenic movement disorders; conversion disorder; Tone was increased, which improved on distraction. chronic fatigue syndrome DAT-SPECT showed reduced tracer uptake in the basal ganglia (Fig. 1a). She was found to have heterozygous de- ------------------------------------------------------------ letion of parkin exon 5 and a duplication of parkin exons Additional Supporting Information may be found in the online version of 2, 3, and 4. After 3 weeks of L-dopa treatment of 300 mg/ this article. day, her motor UPDRS score improved from 56 to 7. She *Correspondence to: Professor Andrew J. Lees, Reta Lila Weston developed limb and trunk chorea within 7 weeks of start- Institute of Neurological Studies, Institute of Neurology, UCL, 1 Wakefield ing treatment (Video 1b). Street, London, WC1N 1PJ, United Kingdom; [email protected]. Relevant conflicts of interest/financial disclosures: Nothing to report. Patient 2 This work was supported by the Reta Lila Weston Trust. Full financial disclosures and author roles may be found in the online This Irish woman presented at age 19 with symptoms version of this article. of fatigue, poor balance, difficulty walking, and quiet Received: 12 September 2010; Revised: 1 November 2010; Accepted: speech. She was reviewed by an immunologist and psy- 8 November 2010 Published online 29 March 2011 in Wiley Online Library chiatrist and was informed she had CFS and depression. (wileyonlinelibrary.com). DOI: 10.1002/mds.23563 Her symptoms gradually deteriorated and became Movement Disorders, Vol. 26, No. 7, 2011 1337 LING ET AL. FIG. 1. (a)[123I]FP-CIT DAT images of patient 1 show absent tracer activity in both putamen nuclei and asymmetrical markedly reduced uptake in both caudate nuclei. (b)[123I]FP-CIT DAT images of patient 2 show markedly reduced uptake in the putamen and asymmetrical reduced uptake in the caudate nuclei. (c)[123I]FP-CIT DAT image of patient 3 shows asymmetrical markedly reduced uptake in the putamen and caudate nuclei. (d) [123I]FP-CIT DAT image of patient 4 shows bilateral reduced tracer uptake in the putamen and caudate nuclei. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.] much worse during pregnancy at age 38. She then devel- GLN100X). She had an excellent response to pramipex- oped right-hand tremor, limb dystonia, gait difficulty, ole. Three years later, L-dopa was started, and peak and frequent falls. Over the next 5 years, she was fol- dose dyskinesia developed within a few months. lowed up in a neurology clinic, but no organic cause was identified. Limb rigidity and brisk reflexes were noted but were considered inconsistent. She was Patient 3 described as being anxious and agitated during consul- At age 33, this Estonian nurse developed low mood, tations. At age 42, she was admitted to the Royal Victo- slowing of movements, and intermittent hand tremor ria Hospital in Belfast, where parkinsonism was a year after a minor car accident. She was diagnosed suspected. During examination, she was very immobile with posttraumatic stress disorder and considered to with gait freezing and postural instability and had have an obsessional, rigid personality with severe asymmetrical cogwheel rigidity, bradykinesia, right- depression by psychiatrists. She developed impairment foot dystonia, and stooped posture (Video 2). DAT- of gait and speech 2 years later and began to require SPECT revealed reduced uptake in both basal ganglia assistance to walk. She remained on antidepressants (Fig. 1b). She was later confirmed to be a compound despite the relentless progression of her motor symp- heterozygote with parkin mutations (ARG275TRP, toms. She was twice admitted to the care of 1338 Movement Disorders, Vol. 26, No. 7, 2011 DELAYED DIAGNOSIS IN MONOGENETIC PARKINSONISM Table 1. Overview of clinical characteristics of patients 1–4 Clinical characteristic Patient 1 Patient 2 Patient 3 Patient 4 Age at onset (y) 31, female 19, female 33, female 28, female Delay in correct diagnosis (y) 14 23 10 12 Presenting complaint Gait freezing Asymmetrical Low mood and slowing Neuroleptic induced bradykinetic rigidity of movements acute dystonic reaction with subsequent development of left leg tremor Predominant motor features Tremulous parkinsonism, Akinetic rigidity, hand Akinetic rigidity, festinant Tremulous parkinsonism, foot dystonia dystonia, gait freezing gait, dysphagia, anarthria postural instability Nonmotor features Fatigue, bradyphrenia, Fatigue, anxiety Low mood Low mood urinary symptoms Functional disability Walked with assistance Severe postural Bedbound, contractures, Walked independently with of 2 sticks instability requiring dysphagia with severe marked postural instability assistance with walking weight loss Genetic findings Compound heterozygote Compound heterozygote PARK1/4 duplication Compound heterozygote parkin mutation parkin mutation carrier of parkin and DJ-1 Features mistakenly identified as supportive of a conversion disorder Distractibility and inconsistency Yes Yes Yes Yes Extreme slowness/florid symptoms Yes No Yes No Paradoxical kinesis Yes No Yes No Health care worker No No Yes Yes Family history of psychiatric illness Yes No No No Variable frequency and amplitude Yes Not performed Yes Not performed on EMG tremor analysis neurologists, at ages 37 and 40. Examination showed she developed gait difficulty and a stooped posture. generalized limb rigidity and slowness of movement, Over 12 years, she was reviewed by 2 neurological with examples of paradoxical kinesis such as normal teams and psychiatrists, all of whom agreed she had reactions in catching a ball. Her gait was described as MCD. At age 40, she was referred to the Department festinant but ‘‘atypical,’’ with knees flexed and short of Neurology at Innsbruck Medical University, Austria, stride length, and she had never fallen. Her speech was where parkinsonism was suspected for the first time. slow and spoken in short sentences. The neurologists on Examination revealed pill-rolling rest tremor in the left both occasions diagnosed an MCD. At age 43, she hand, asymmetrical rigidity, and bradykinesia. She became bedbound and developed dysphagia, resulting in walked independently with small steps and had marked severe weight loss. She was admitted to the University postural instability. A dose of 300 mg/day of L-dopa Hospital of Tartu in Estonia, where an organic cause of led to complete
Recommended publications
  • Epidemic Encephalitis Etiology and Sequelae
    University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1936 Epidemic encephalitis etiology and sequelae Alice G. Hildebrand University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Hildebrand, Alice G., "Epidemic encephalitis etiology and sequelae" (1936). MD Theses. 441. https://digitalcommons.unmc.edu/mdtheses/441 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. EPIDEMIC ENCEPHALITIS ETIOLOGY and SEQUELAE Compiled by: Alice Grace Hildebrand. SENIOR THESIS 1936 University of Nebraska, College of Medicine, Omaha, Nebr. 480772 TABLE OF COlJTENTS I. Introduction ........................................ • 1 II. Historical Outbreaks and Recent Epidemics •••••••••••• 3 III. Etiology: 1. General Factors •••••••••••••••••••••••••••••••••• 12 2. Relationship to Other Diseases ••••••••••••••••••• 17 3. Toxic Disturbances of Central Nervous System ••••• 23 4. Cultivatable Bacteria •••••••••••••••••••••••••••• 25 5. Filtrable Viruses ••••••••••••••••••••••••••••••••32 IV. Sequelae: 1. Int~oduction •••••••••••••••••••••••••••••••••••••48 2. Mental
    [Show full text]
  • Dystonia and Chorea in Acquired Systemic Disorders
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.65.4.436 on 1 October 1998. Downloaded from 436 J Neurol Neurosurg Psychiatry 1998;65:436–445 NEUROLOGY AND MEDICINE Dystonia and chorea in acquired systemic disorders Jina L Janavs, Michael J AminoV Dystonia and chorea are uncommon abnormal Associated neurotransmitter abnormalities in- movements which can be seen in a wide array clude deficient striatal GABA-ergic function of disorders. One quarter of dystonias and and striatal cholinergic interneuron activity, essentially all choreas are symptomatic or and dopaminergic hyperactivity in the nigros- secondary, the underlying cause being an iden- triatal pathway. Dystonia has been correlated tifiable neurodegenerative disorder, hereditary with lesions of the contralateral putamen, metabolic defect, or acquired systemic medical external globus pallidus, posterior and poste- disorder. Dystonia and chorea associated with rior lateral thalamus, red nucleus, or subtha- neurodegenerative or heritable metabolic dis- lamic nucleus, or a combination of these struc- orders have been reviewed frequently.1 Here we tures. The result is decreased activity in the review the underlying pathogenesis of chorea pathways from the medial pallidus to the and dystonia in acquired general medical ventral anterior and ventrolateral thalamus, disorders (table 1), and discuss diagnostic and and from the substantia nigra reticulata to the therapeutic approaches. The most common brainstem, culminating in cortical disinhibi- aetiologies are hypoxia-ischaemia and tion. Altered sensory input from the periphery 2–4 may also produce cortical motor overactivity medications. Infections and autoimmune 8 and metabolic disorders are less frequent and dystonia in some cases. To date, the causes. Not uncommonly, a given systemic dis- changes found in striatal neurotransmitter order may induce more than one type of dyski- concentrations in dystonia include an increase nesia by more than one mechanism.
    [Show full text]
  • Acute and Chronic Chorea in Childhood Donald L
    Acute and Chronic Chorea in Childhood Donald L. Gilbert, MD, MS This review discusses diagnostic evaluation and management of chorea in childhood. Chorea is an involuntary, hyperkinetic movement disorder characterized by continuous, jerky, or flowing movement fragments, with irregular timing and direction. It tends to be enhanced by voluntary actions and generally causes interference with fine motor function. The diagnostic evaluation begins with accurate classification of the movement disorder followed by consideration of the time course. Most previously healthy children presenting with acute/subacute chorea have an autoimmune etiology. Chronic chorea usually occurs as part of encephalopathies or diseases causing more global neurologic symptoms. We review the management of acute/subacute and chronic choreas, with special emphasis on Sydenham chorea and benign hereditary chorea. Semin Pediatr Neurol 16:71–76 © 2009 Published by Elsevier Inc. horea is a nonpatterned, involuntary, hyperkinetic genetic chorea, will be emphasized. Paroxysmal movement Cmovement disorder. It is continuous, variable in speed, disorders involving chorea will not be discussed but are re- unpredictable in timing and direction, and flowing or jerky in viewed elsewhere.4 As the phenomenology of chorea over- appearance.1 Chorea may be accompanied by athetosis or laps in acute and chronic choreas, most features of the neu- ballism. Athetosis is also continuous but the rate is slower. rologic examination will be discussed under acute chorea. Athetosis often accompanies dystonia or occurs in symptom- atic chorea and may be referred to as choreoathetosis. Ballism designates larger amplitude, flinging, proximally generated Acute Chorea movements. It rarely occurs in isolation in children but can accompany chorea.
    [Show full text]
  • Fatigue and Parkinson's Disease
    Fatigue and Parkinson’s Disease Gordon Campbell MSN FNP PADRECC Portland VAMC, October 24, 2014 Sponsored by the NW PADRECC - Parkinson's Disease Research, Education & Clinical Center Portland VA Medical Center www.parkinsons.va.gov/Northwest Outline • What is fatigue? • How differs from sleepiness, depression • How do doctors measure it? • Why is fatigue such a problem in PD? • How if fatigue in PD different? • How will exercise and nutrition help? • Will medications work? What is Fatigue? • One of most common symptoms in medicine. • Fatigue is the desire to rest. No energy. • Chronic fatigue: “overwhelming and sustained exhaustion and decreased capacity to physical or mental work, not relieved by rest • Acute (days) or chronic (months, years) • May be incapacitating • Cannot be checked with doctor’s exam – Not like tremor, stiffness 1 Fatigue: What Is It? • Not sleepiness (cannot stay awake) • Not depression (blue, hopeless, cranky) • Rather is sustained exhaustion and decreased capacity for physical and mental work that is not relieved by rest – Get up tired after a night's sleep, always tired. • Also, a subjective lack of physical and/or mental energy that interferes with usual and desired activities Fatigue: A Big Problem • 10 million physician office visits/year in USA. • Usual cause for this fatigue in general doctor’s office = depression. • Different in Parkinson’s disease, various other medical illnesses. 2 Many Illnesses and Drugs Cause Fatigue • Medical diseases – Diabetes – Thyroid disease (too low or too high) – Emphysema, heart failure – Rheumatologic diseases – Cancer or radiation therapy – Anemia • Drugs – Beta blockers, antihistamines, pain killers, alcohol • Other neurological diseases – Strokes – Post polio syndrome – Narcolepsy, obstructive sleep apnea – Old closed head injuries – Multiple sclerosis 5 Dimensions of Fatigue • General fatigue • Physical fatigue • Mental fatigue • Reduced motivation • Reduced activity Depression correlates with all 5 dimensions.
    [Show full text]
  • Brain Imaging Reveals Clues About Chronic Fatigue Syndrome 23 May 2014
    Brain imaging reveals clues about chronic fatigue syndrome 23 May 2014 The results are scheduled for publication in the journal PLOS One. "We chose the basal ganglia because they are primary targets of inflammation in the brain," says lead author Andrew Miller, MD. "Results from a number of previous studies suggest that increased inflammation may be a contributing factor to fatigue in CFS patients, and may even be the cause in some patients." Miller is William P. Timmie professor of psychiatry and behavioral sciences at Emory University School of Medicine. The study was a collaboration among researchers at Emory University School of Medicine, the CDC's Chronic Viral Diseases Branch, and the University of Modena and Reggio Credit: Vera Kratochvil/public domain Emilia in Italy. The study was funded by the CDC. The basal ganglia are structures deep within the brain, thought to be responsible for control of A brain imaging study shows that patients with movements and responses to rewards as well as chronic fatigue syndrome may have reduced cognitive functions. Several neurological disorders responses, compared with healthy controls, in a involve dysfunction of the basal ganglia, including region of the brain connected with fatigue. The Parkinson's disease and Huntington's disease, for findings suggest that chronic fatigue syndrome is example. associated with changes in the brain involving brain circuits that regulate motor activity and In previous published studies by Emory motivation. researchers, people taking interferon alpha as a treatment for hepatitis C, which can induce severe Compared with healthy controls, patients with fatigue, also show reduced activity in the basal chronic fatigue syndrome had less activation of the ganglia.
    [Show full text]
  • Fatigue After Stroke
    SPECIAL REPORT Fatigue after stroke PJ Tyrrell Fatigue is a common symptom after stroke. It is not invariably related to stroke severity & DG Smithard† and can occur in the absence of depression. It is one of the most troublesome symptoms for †Author for correspondence many patients and yet nothing is known of its causation. There are no specific treatments. William Harvey Hospital, Richard Steven’s Ward, This article assesses the available literature in the context of what is known about fatigue Ashford, Kent, in other disorders. Post-stroke fatigue may be a manifestation of sickness behavior, TN24 0LZ, UK mediated through the central effects of the cytokine interleukin-1, perhaps via effects on Tel.: +44 123 361 6214 Fax: +44 123 361 6662 glutamate neurotransmission. Possible therapeutic strategies are discussed which might be [email protected] a logical basis from which to plan randomized control trials. Following stroke, approximately a third of common and disabling symptom of Parkinson’s patients die, a third recover and a third remain disease [7,8] and of systemic lupus [9]. More than significantly disabled. Even those who recover 90% of patients with poliomyelitis develop a physically may be left with significant emotional delayed syndrome of post-myelitis fatigue [10]. and psychologic dysfunction – including anxi- Fatigue is the most prevalent symptom of ety, readjustment reactions and depression. One patients with cancer who receive radiation, cyto- common but often overlooked symptom is toxic or other therapies [11], and it may persist fatigue. This may occur soon or late after stroke, for years after the cessation of treatment [12].
    [Show full text]
  • Wilson's Disease
    Reprinted with permission from Thieme Medical Publishers (Semin Neurol. 2007 April;27(2):123-132) Homepage at www.thieme.com Wilson’s Disease Ronald F. Pfeiffer, M.D.1 ABSTRACT Wilson’s disease is an autosomal-recessive disorder caused by mutation in the ATP7B gene, with resultant impairment of biliary excretion of copper. Subsequent copper accumulation, first in the liver but ultimately in the brain and other tissues, produces protean clinical manifestations that may include hepatic, neurological, psychiatric, oph- thalmological, and other derangements. Genetic testing is impractical because of the multitude of mutations that have been identified, so accurate diagnosis relies on judicious use of a battery of laboratory and other diagnostic tests. Lifelong palliative treatment with a growing stable of medications, or with liver transplantation if needed, can successfully ameliorate or prevent the progressive deterioration and eventual death that would otherwise inevitably ensue. This article discusses the epidemiology, genetics, pathophysi- ology, clinical features, diagnostic testing, and treatment of Wilson’s disease. KEYWORDS: Ceruloplasmin, copper, Wilson’s disease, penicillamine, zinc Although he was not the first to recognize the EPIDEMIOLOGY disease process,1 in a doctoral thesis of more than 200 Wilson’s disease is a rare autosomal-recessive disorder. A pages published in Brain in 1912, S. A. Kinnier Wilson prevalence rate of 30 cases per million (or one per masterfully provided the first detailed, coherent descrip- 30,000) and a birth incidence rate of one per 30,000 to 12–15 tion of both the clinical and pathological details of the 40,000 are often quoted. It has been estimated that entity that now bears his name.2 Many other individuals there are 600 cases of Wilson’s disease in the United 14 have embellished and expanded our understanding of States and that 1% of the population are carriers.
    [Show full text]
  • Abnormal Eye Movements in Three Types of Chorea
    DOI: 10.1590/0004-282X20160109 VIEW AND REVIEW Abnormal eye movements in three types of chorea Anormalidades dos movimentos oculares em três tipos de coreia Tiago Attoni1, Rogério Beato2, Serge Pinto3, Francisco Cardoso2 ABSTRACT Chorea is an abnormal movement characterized by a continuous flow of random muscle contractions. This phenomenon has several causes, such as infectious and degenerative processes. Chorea results from basal ganglia dysfunction. As the control of the eye movements is related to the basal ganglia, it is expected, therefore, that is altered in diseases related to chorea. Sydenham’s chorea, Huntington’s disease and neuroacanthocytosis are described in this review as basal ganglia illnesses that can present with abnormal eye movements. Ocular changes resulting from dysfunction of the basal ganglia are apparent in saccade tasks, slow pursuit, setting a target and anti-saccade tasks. The purpose of this article is to review the main characteristics of eye motion in these three forms of chorea. Keywords: chorea; eye movements; Huntington disease; neuroacanthocytosis. RESUMO Coreia é um movimento anormal caracterizado pelo fluxo contínuo de contrações musculares ao acaso. Este fenômeno possui variadas causas, como processos infecciosos e degenerativos. A coreia resulta de disfunção dos núcleos da base, os quais estão envolvidos no controle da motricidade ocular. É esperado, então, que esta esteja alterada em doenças com coreia. A coreia de Sydenham, a doença de Huntington e a neuroacantocitose são apresentadas como modelos que têm por característica este distúrbio do movimento, por ocorrência de processos que acometem os núcleos da base. As alterações oculares decorrentes de disfunção dos núcleos da base se manifestam em tarefas de sacadas, perseguição lenta, fixação de um alvo e em tarefas de antissacadas.
    [Show full text]
  • ME/CFS) Key Facts
    KEY FACTS FEBRUARY 2015 For more information visit www.iom.edu/MECFS Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) Key Facts What is the prevalence of ME/CFS? • ME/CFS affects 836,000 to 2.5 million Americans. • An estimated 84 to 91 percent of people with ME/CFS have not yet been diagnosed, meaning the true prevalence of ME/CFS is unknown. • ME/CFS affects women more often than men. Most patients currently diagnosed with ME/CFS are Caucasian, but some studies suggest that ME/CFS is more common in minority groups. • The average age of onset is 33, although ME/CFS has been reported in patients younger than age 10 and older than age 70. What are the symptoms and other effects of ME/CFS? • There are five main symptoms of ME/CFS: 1. Reduction or impairment in ability to carry out normal daily activities, accompanied by pro- found fatigue; 2. Post-exertional malaise (worsening of symptoms after physical, cognitive, or emotional effort); 3. Unrefreshing sleep; 4. Cognitive impairment; and 5. Orthostatic intolerance (symptoms that worsen when a person stands upright and improve when the person lies back down). • Other common manifestations of ME/CFS include pain, failure to recover from a prior infection, and abnormal immune function. • At least one-quarter of ME/CFS patients are bed- or house-bound at some point in their illness. • Symptoms can persist for years, and most patients never regain their pre-disease level of health or functioning. • ME/CFS patients experience loss of productivity and high medical costs that contribute to a total economic burden of $17 to $24 billion annually.
    [Show full text]
  • HEADACHES and ME/CFS INTRODUCTION Headaches Are Often Reported by People with ME/CFS
    MANAGEMENT FILE the ME association by DR CHARLES SHEPHERD, our medical adviser This leaflet is based on an article which first appeared in the ME Association’s quarterly ME Essential magazine. MEA membership costs £18 a year for people living in the UK/BFPO. For contact details, see foot of this page. February 2020 HEADACHES AND ME/CFS INTRODUCTION Headaches are often reported by people with ME/CFS. They also form part of the symptom list for most diagnostic criteria for ME/CFS. But headaches can obviously have other causes – physical and psychological – as well. WHAT CAUSES HEADACHES? Doctors classify headaches as being sides of the head – as if a rubber band arteries in the head and neck. primary where there is no obvious link has been stretched around it. Common Temporal arteritis is a medical to an underlying medical problem, or causes include stress, depression, lack emergency that requires urgent treat- secondary where there is a clear link. of proper sleep, skipping meals, not ment with high-dose steroids. drinking enough fluid and alcohol. Primary headaches include: Headaches in women can be caused Secondary headaches are caused by Cluster headaches by hormonal problems – including an existing medical problem. Some of An excruciatingly painful headache taking the contraceptive pill, going these are serious, which is why you must that causes intense pain around one through the menopause, pregnancy, see your doctor if you have severe or eye. Cluster headaches are fairly rare and as part of period pain. persistent headaches. and tend to occur in clusters for a It’s also worth noting that a headache month or two, sometimes around the Common causes, which are normally is the most common symptom of same time each year.
    [Show full text]
  • Chronic Fatigue Syndrome (CFS) Disease Fact Sheet Series
    WISCONSIN DIVISION OF PUBLIC HEALTH Department of Health Services Chronic Fatigue Syndrome (CFS) Disease Fact Sheet Series What is chronic fatigue syndrome? Chronic fatigue syndrome (CFS) is a recently defined illness consisting of a complex of related symptoms. The most characteristic symptom is debilitating fatigue that persists for several months. What are the other symptoms of CFS? In addition to profound fatigue, some patients with CFS may complain of sore throat, slight fever, lymph node tenderness, headache, muscle and joint pain (without swelling), muscle weakness, sensitivity to light, sleep disturbances, depression, and difficulty in concentrating. Although the symptoms tend to wax and wane, the illness is generally not progressive. For most people, symptoms plateau early in the course of the illness and recur with varying degrees of severity for at least six months and sometimes for several years. What causes CFS? The cause of CFS is not yet known. Early evidence suggested that CFS might be associated with the body's response to an infection with certain viruses, however subsequent research has not shown an association between an infection with any known human pathogen and CFS. Other possible factors that have been suspected of playing a role in CFS include a dysfunction in the immune system, stress, genetic predisposition, and a patient’s psychological state. Is CFS contagious? Because the cause of CFS remains unknown, it is impossible to answer this question with certainty. However, there is no convincing evidence that the illness can be transmitted from person to person. In fact, there is no indication at this time that CFS is caused by any single recognized infectious disease agent.
    [Show full text]
  • Neurology A.N
    Postgrad Med J (1991) 67, 509 - 531 i) The Fellowship of Postgraduate Medicine, 1991 Postgrad Med J: first published as 10.1136/pgmj.67.788.509 on 1 June 1991. Downloaded from Reviews in Medicine Neurology A.N. Gale, J.M. Gibbs, A.H.V. Schapira and P.K. Thomas Department ofNeurological Science, Royal Free Hospital School ofMedicine, RowlandHill Street, London NW3 2PF, UK Introduction The past few years have seen a significant improve- gitis, Tunkel et al.' point out that the mortality has ment in our ability to diagnose and treat neuro- not changed significantly over the last 30 years but logical diseases. New imaging techniques such as the prognosis for Gram-negative meningitis has computed tomographic (CT) scanning and magne- been markedly improved by the introduction of tic resonance imaging (MRI) have had a major third generation cephalosporins. impact on the practice ofneurology. Whilst techni- In adults and older children the commonest ques such as positron emission tomography (PET) causative organisms are Neisseria meningitidis and are mainly research orientated at present, they may Streptococcus pneumoniae and the treatment of soon find wider clinical application. New electro- choice in the UK is intravenous benzyl penicillin, physiological examinations such as magnetic brain with chloramphenicol as a second line agent. In stimulation have found use in the investigation of children aged 4 months to 6 years the most likely central motor conduction pathways. The applica- organism is Haemophilus influenzae type b which copyright. tion of the techniques of molecular biology to the may be resistant to ampicillin. Initial treatment in study of neurological disease is having a profound this age group has been chloramphenicol and effect on our understanding of the mechanisms ampicillin until sensitivities are known, but Peltona underlying these diseases.
    [Show full text]