DOCSLIB.ORG

Correspondence

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Correspondence THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES Correspondence ASSOCIATION BETWEEN ALZHEIMER DISEASE AND This work was supported by the Alzheimer Society of British AMYOTROPHIC LATERAL SCLEROSIS? Columbia. A.D. Sadovnick Department of Medical Genetics To the Editor: 1 U.B.C. I read with interest the recent article by Frecker et al dis­ Vancouver, B.C. cussing the possible association between Alzheimer disease (AD) and amyotrophic lateral sclerosis (ALS). 1. Frecker MF, Fraser FC, Andermann E, et al. Associalion belween Alzheimer Disease and Amyotrophic Lateral Sclerosis? Can J To date, 617 consecutive, unrelated index cases attending the Neurol Sci 1990; 17: 12-14. Clinic for Alzheimer Disease and Related Disorders have had 2. Andreasen NC, Edicott J, Spitzer RL. The family history method detailed family histories taken using the family history method using diagnostic criteria: reliability and validity. Arch Gen 2 Psychiatry 1977; 34: 1229-1235. with multiple informants. Three relatives of 2 out of 233 3. McKahnn G, Drachman D, Folstein M, et al. Clinical diagnosis of (0.86%) index cases with a diagnosis of "probable" AD accord­ Alzheimer's disease: report of the NINCDS-ADRDA Work ing to recognized criteria3 possibly had ALS. Group under the auspices of the Department of Health and Family "A" was of Norweigan ancestry. The index case, the Human Services Task Force on Alzheimer's disease. Neurology 1984; 34: 939-44. eldest of 2 children, had the onset of her dementia at approxi­ 4. Kurtzke KF. Epidemiology of amyotrophic lateral sclerosis. In: mately age 50. She is still alive at age 55. Her sister, aged 44, is Rowland LP, ed. Human Motor Neuron Diseases. New York: alive and well. Her father died at age 66 from a brain tumor and Raven Press 1982; 281-302. was mentally alert. Her mother died at age 62 and the diagnosis of ALS in this lady was confirmed by autopsy. There was one POSSIBLE INTERACTIONS BETWEEN DEPRENYL maternal uncle (brother of the index case's mother) who report­ AND PROZAC edly suffered from dementia and ALS. An autopsy performed in 1974 confirmed the diagnosis of ALS, but the etiology of the To the Editor: dementia was not resolved. Fluoxetine (Prozac) and Selegiline (Deprenyl), are two new Family "B" was of English ancestry. The index case, the medications which have only recently been introduced on the youngest of four children, had the onset of her dementia at age North American market. There is limited experience using these 72. She is still alive at age 79. One of her brothers died at age 18 medications in combination, and we would like to describe two during World War II and another brother died at age 75 from patients in which there may have been an interaction between heart problems and was mentally alert until his death. Her sister these two drugs. also developed dementia at age 72 and died at age 77 with a The first patient is a 46-year-old woman, with moderately neuropathologically confirmed diagnosis of AD. The index severe, left sided Parkinson's disease, who was maintained on case's father died at age 86 and was mentally alert until his Prolopa 15/12.5 every two hours and bromocriptine 10 mg t.i.d. death. Family informants reported that her mother had a "neuro­ She was also taking amitriptyline 50 mg hs for depression, logical condition", but all relevant clinical records on this lady which over the years had been considered to be an atypical have been destroyed. However, clinical records on the index depression. She had taken selegiline for a month in the fall of case's sister were obtained. These stated that "her mother died at 1989, but discontinued it because of lack of perceived benefit. age 67, secondary to some neurological disease that sounds sim­ In January of 1990, because of anticholinergic side-effects, ilar to ALS". the amitriptyline was discontinued and fluoxetine 20 mg q.a.m. One hundred forty-six index cases seen at the Clinic are initiated. Selegiline was re-started about ten days later. Initially, presently diagnosed as "possible" AD.3 Of these, informants for the patient felt much better. However the next month, she one family reported a relative with ALS. Family "C" was of became increasingly hyperactive, over communicative, elated German, Dutch and English ancestry. The index case, the sec­ and creative. Her actions and judgement appeared grossly ond of four children, had the onset of her dementia at age 62 and impaired, and her physicians thought her to be manic. Both the is still alive at age 67. Her eldest sister died in her mid-fifties selegiline and fluoxetine were discontinued, and the patient from a brain tumor. Another sister is alive and well at age 65. slowly improved, over the next 2 months. Her only brother died at approximately age 60 from ALS, diag­ Fluoxetine has previously been reported to cause mania1-2 nosed clinically but there was no autopsy. although usually at higher doses than 20 mg a day, and manic In summary, out of 379 consecutive, unrelated index cases symptoms resolved quickly with discontinuation of fluoxetine. with a diagnosis of "probable" or "possible" AD,3 3 (0.79%) had Selegiline is metabolized to 1-amphetamine and 1-metham- a total of 4 first- or second-degree relatives reported to have phetamine, and may cause agitation in some patients. In one ALS. Assuming a prevalence for ALS of 1 in 100.000,4 this is case, selegiline alone was reported to cause manic behavior.3 more frequent than expected. We therefore agree with Frecker Thus, the severe prolonged mania seen in this patient may have and colleagues' that further investigation is warranted on the been due to the concomitant use of selegiline and fluoxetine. possible association between ALS and AD. The second patient, a 56-year-old woman, with moderate 352 Downloaded from https://www.cambridge.org/core. IP address: 170.106.35.234, on 24 Sep 2021 at 10:21:48, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0317167100030730 LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES Parkinson's disease, had selegiline 5 mg q.a.m. added to her pre­ DR. McKENZIE'S YEAR WITH DR. CUSHING vious regime of Parlodel 5 mg t.i.d. and Sinemet 100/25, 8 tablets per day in January of 1990. She was also on amitripty- To the Editor: line, for depression which was discontinued in March of 1990 Dr. Kenneth McKenzie and his many contributions to the art because of urinary hesitancy. The patient was started on fluoxe­ of neurosurgery are long remembered even after half a century. tine 20 mg q.a.m. After receiving a degree in medicine from the University of Toronto in 1914, he joined the British Royal Medical Corps Several days after starting the fluoxetine, the patient started when World War I was declared. After the war, he returned to to develop episodes, during which she would shiver and break the University of Toronto for postgraduate surgical training with out into a cold sweat. The episodes would start in midafternoon, Dr. Clarence L. Starr, the Professor and Chief of Surgery there. and last for several hours. On these occasions, she would feel When Dr. Harvey Cushing was awarded the Charles Mickle very clammy, and her hands would be cold. She was seen in the Fellowship by the University of Toronto in 1922, he invited Dr. office for assessment one month later. At that time, it was noted Starr to send a man to Boston to train with him in neurosurgery. that she was very diaphoretic. Her hands were severely vasocon- Dr. McKenzie was selected for the position and given a $1000 stricted, and the fingers were blue and mottled. Her blood pres­ scholarship.1 sure was 200/120. Dr. McKenzie's contributions during his career were numer­ Previously, the patient had had transient elevations of blood ous and included operative modifications and improvements in pressure, which were usually induced by stress, but she did not the treatment of chronic subdural hematomas and gliomas. He feel under stress on this occasion. The selegiline and fluoxetine seemed to take particular interest in pathological conditions were both discontinued, and she recovered over the next few affecting the cranial nerves. For example he studied and wrote days. Her blood pressure returned to normal (120/90). She did about Menier's disease, acoustic neuromas, and spasmodic torti­ not have any further diaphoretic episodes. She has since restart­ collis. In reviewing the surgical histories of the Peter Bent ed fluoxetine with no side-effects. Brigham Hospital (PBBH) from 1922 to 1923, we have found This patient developed a very unusual reaction, which has that Dr. McKenzie was also interested in the treatment of not been reported previously with either selegiline or fluoxetine. trigeminal neuralgia. During Dr. McKenzie's training period in As she was able to tolerate both medications independently, it Boston, Dr. Harvey Cushing and Dr. Gilbert Horrax performed would appear to be specifically due to this combination. many operations for the treatment of trigeminal neuralgia. Dr. Selegiline, a selective MAOB inhibitor at low doses (5- McKenzie performed admission neurological examinations on 10 mg a day) has been reported to cause hypertension, when most of these patients and recorded both objective and subjec­ taken in high doses, due to loss of selectivity.4 However, this tive findings for each cranial nerve. He then documented many patient was taking only 5 mg a day and use of deprenyl alone of his post-operative neurological examinations with diagrams did not cause any elevation of BP on previous visits.
Load more

Recommended publications
  • Canadian Stroke Best Practice Recommendations
    CANADIAN STROKE BEST PRACTICE RECOMMENDATIONS MOOD, COGNITION AND FATIGUE FOLLOWING STROKE Table 1C: Summary Table for Selected Pharmacotherapy for Post-Stroke Depression Update 2019 Lanctôt KL, Swartz RH (Writing Group Chairs) on Behalf of the Canadian Stroke Best Practice Recommendations Mood, Cognition and Fatigue following Stroke Writing Group and the Canadian Stroke Best Practice and Quality Advisory Committee, in collaboration with the Canadian Stroke Consortium © 2019 Heart & Stroke Heart and Stroke Foundation Mood, Cognition and Fatigue following Stroke Canadian Stroke Best Practice Recommendations Table 1C Table 1C: Summary Table for Selected Pharmacotherapy for Post-Stroke Depression This table provides a summary of the pharmacotherapeutic properties, side effects, drug interactions and other important information on selected classes of medications available for use in Canada and more commonly recommended for post-stroke depression. This table should be used as a reference guide by health care professionals when selecting an appropriate agent for individual patients. Patient compliance, patient preference and/or past experience, side effects, and drug interactions should all be taken into consideration during decision-making, in addition to other information provided in this table and available elsewhere regarding these medications. Selective Serotonin Reuptake Inhibitors (SSRI) Serotonin–norepinephrine reuptake Other inhibitors (SNRI) Medication *citalopram – Celexa *duloxetine – Cymbalta methylphenidate – Ritalin (amphetamine)
    [Show full text]
  • The Pharma-Fever That Almost Got Away
    EMERGENCY MEDICINE RESIDENCY CPC The pharma-fever that almost got away XIAO CHI ZHANG, MD, MS; MATTHEW SIKET, MD; WILLIAM BINDER, MD 29 31 EN From the Case Records of the Alpert Medical School of DR. SARAH GAINES: A fever greater than 41.0°C is quite Brown University Residency in Emergency Medicine elevated and unusual. Is this dangerous? What was your differential? DR. XIAO CHI ZHANG: A 68-year-old man was brought into DR. MATTHEW SIKET: Humans generally tolerate tempera- the Emergency Department by his family with chills and tures below 41° C (105.8° F). In contrast to hyperthermia, in altered mental status. Two days prior to his ED presenta- which an imbalance between heat generation versus dissipa- tion, the patient had an episode in which he “spaced-out” tion occurs without up-regulation of the hypothalamic set and was unable to comprehend or acknowledge his wife. She point, fever as a host defense against infection rarely reaches reported that he did not have any signs of seizure activity dangerous levels in neurologically competent individuals. and did not have any focal weakness. The episode lasted Very high temperatures can be related to urosepsis, intraab- approximately 30 minutes and he returned to his baseline. dominal sepsis, C. difficile colitis, meningitis, and central Today he had another episode, but this time associated with venous catheter infections. Hyperpyrexia, defined as tem- chills and rigors. His past medical history was significant perature > 41.5°C (106.7°F) is an uncommon result of infec- for chronic back pain due to bony metastasis from Stage IV tion and usually implies central fever, neurologic malignant non-small cell lung adenocarcinoma, requiring palliative syndrome, malignant hyperthermia, adrenal insufficiency, gamma knife radiation, as well as a daily oral chemotherapy or a drug related cause.1 Our patient was hyperpyrexic, sug- agent, erlotinib, an oral tyrosine kinase inhibitor.
    [Show full text]
  • PRESCRIBED DRUGS and NEUROLOGICAL COMPLICATIONS K a Grosset, D G Grosset Iii2
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.2004.045757 on 16 August 2004. Downloaded from PRESCRIBED DRUGS AND NEUROLOGICAL COMPLICATIONS K A Grosset, D G Grosset iii2 J Neurol Neurosurg Psychiatry 2004;75(Suppl III):iii2–iii8. doi: 10.1136/jnnp.2004.045757 treatment history is a fundamental part of the healthcare consultation. Current drugs (prescribed, over the counter, herbal remedies, drugs of misuse) and how they are taken A(frequency, timing, missed and extra doses), drugs tried previously and reason for discontinuation, treatment response, adverse effects, allergies, and intolerances should be taken into account. Recent immunisations may also be of importance. This article examines the particular relevance of medication in patients presenting with neurological symptoms. Drugs and their interactions may contribute in part or fully to the neurological syndrome, and treatment response may assist diagnostically or in future management plans. Knowledge of medicine taking behaviour may clarify clinical presentations such as analgesic overuse causing chronic daily headache, or severe dyskinesia resulting from obsessive use of dopamine replacement treatment. In most cases, iatrogenic symptoms are best managed by withdrawal of the offending drug. Indirect mechanisms whereby drugs could cause neurological problems are beyond the scope of the current article—for example, drugs which raise blood pressure or which worsen glycaemic control and consequently increase the risk of cerebrovascular disease, or immunosupressants
    [Show full text]
  • Catatonia, NMS, and Serotonin Syndrome
    Catatonia, NMS, and Serotonin Syndrome Christopher M. Celano, MD, FACLP Associate Director, Cardiac Psychiatry Research Program, Massachusetts General Hospital Assistant Professor of Psychiatry, Harvard Medical School October 22, 2020 www.mghcme.org Disclosure: Christopher Celano, MD Sunovion Company Pharmaceuticals Employment Management Independent Contractor Consulting Speaking & Teaching I Board, Panel or Committee Membership D – Relationship is considered directly relevant to the presentation I – Relationship is NOT considered directly relevant to the presentation www.mghcme.org Catatonia: How common is it? • 7.8-9.0% prevalence rate – Highest rates in non-psychiatric (i.e., medical) settings and in patients undergoing ECT. • 1.6-5.5% of all patients seen on psychiatry consultation service – Prevalence higher for older patients • Up to 46% of cases may have etiology that is not primarily psychiatric Grover 2015, Carroll 1994, Jaimes-Albornoz 2013, Fricchione 2008 www.mghcme.org When are you called? • Staff reports the patient is “Playing POSSUM” • Perseveration (speech or behavior) • Oppositionality to all requests • Speech that trails off or is whispereD • Slowed response to questions or commands • Undernourished (reports of decreased PO intake) • Motionless but awake www.mghcme.org Diagnosing Catatonia: DSM-5 DSM-5 requires 3 or more of the following: • Catalepsy • Posturing • Waxy flexibility • Mannerisms • Stupor • Stereotypies • Agitation • Grimacing • Mutism • Echolalia • Negativism • Echopraxia American Psychiatric Association 2013 www.mghcme.org Bush-Francis Rating Scale • Excitement • VerBigeration • Immobility/stupor • Rigidity • ComBativeness • Negativism • Autonomic Abnormality • Waxy flexiBility • Impulsivity • Withdrawal • Mutism • Automatic OBedience • Staring • Mitgehen • Posturing/catalepsy • Gegenhalten • Grimacing • AmBitendency • Echopraxia/echolalia • Grasp Reflex • Stereotypy • Perseveration • Mannerisms Bush 1996 www.mghcme.org Challenges with Diagnosis • Clarifying specific symptoms can be difficult – Rigidity vs.
    [Show full text]
  • Triptan Therapy for Acute Migraine
    Triptan Therapy for Acute Migraine Headache John Farr Rothrock, MD University of Alabama at Birmingham, Birmingham, AL Deborah I. Friedman, MD, MPH University of Texas Southwestern, Dallas, TX The “triptans” are 5HT-1B/1D receptor agonists that were developed to treat acute migraine and acute cluster headache. Sumatriptan, the original triptan preparation, has been in general use since 1993, so there has been considerable experience with triptans over time. There are currently seven oral triptans on the market in the United States: sumatriptan (Imitrex™), naratriptan (Amerge™), zolmitriptan (Zomig™), rizatriptan (Maxalt™), almotriptan (Axert™), frovatriptan (Frova™), and eletriptan (Relpax™); brand names may differ by country. There is also a combination preparation of oral sumatriptan/naproxen (Treximet™). Two triptans (sumatriptan, zolmitriptan) are marketed as nasal sprays, and sumatriptan is available for subcutaneous injection, including a needle-free subcutaneous delivery system (Sumavel™). Sumatriptan suppositories are marketed in Europe but not in North America. Zolmitriptan and rizatriptan are sold in an oral disintegrating tablet or “melt” formulation as well as in tablet form; while the “melt” formulations may be more convenient (no liquid is required to propel them into the stomach), they are absorbed similarly to regular tablets and there is no evidence to suggest that they work faster than the tablet formulations. Some patients with migraine-associated nausea prefer the disintegrating tablets while others cannot tolerate their taste. Although all of the triptans initially were investigated for the treatment of migraine headache of moderate to severe intensity and were superior to placebo in those pivotal trials, they appear to be more consistently effective when used to treat migraine earlier in the attack, when the headache is still mild to moderate.
    [Show full text]
  • Neuroleptic Malignant Syndrome Vs Serotonin Syndrome: Can They Be Distinguished Without an Underlying Etiology?
    Neuroleptic Malignant Syndrome vs Serotonin Syndrome: Can They Be Distinguished Without an Underlying Etiology? Roy R. Reeves, DO, PhD; Mark E. Ladner, MD; and Percy Smith, PA The potentially serious complications for patients with neuroleptic malignant syndrome and serotonin syndrome cannot be underplayed by mental health clinicians, patients, and their families. The authors discuss clinical similarities and diagnostic and treatment approaches to the 2 syndromes. euroleptic malignant syn- of symptoms or whether the patient ployment. He had stopped taking his drome (NMS) and sero- was taking different medications that medication (risperidone 3-mg daily) tonin syndrome (SS) are rare could affect both the serotonin and 3 months earlier, because he was Nbut potentially fatal condi- dopamine systems. experiencing adverse effects (AEs) tions associated with the treatment In clinical practice many patients and shortly thereafter hearing voices. of psychotropic medications. Neu- are treated concurrently with both The clinic psychiatrist started him on roleptic malignant syndrome is be- dopamine receptor antagonists and olanzapine 10-mg daily and sertra- lieved to be caused by a reduction in agents that increase serotonin activity. line 50-mg daily. At a follow-up visit dopaminergic activity secondary to Thus, the distinction of NMS and SS a week later, Mr. A showed an im- drug-induced dopaminergic block- may be problematic if these patients provement of his mood and reported age, whereas SS results from an ex- develop symptoms that could be at- that his hallucinations had decreased cess of central nervous system (CNS) tributed to either disorder. This article significantly. serotonin activity, usually because will discuss the clinical similarities of Several days later, Mr.
    [Show full text]
  • JAMA Neurology Pages 525-636
    In This Issue May 2018 Volume 75, Number 5 JAMA Neurology Pages 525-636 Research Opinion Amyloid and Tau Accumulation in Young Adults With ADAD 548 Viewpoint 531 Preventing Sudden Unexpected Although the medial temporal lobe is typically the first area of neurofibrillary tangle depo- Death in Epilepsy sition in aging populations, it is not clear if this is the case for younger individuals who are O Devinsky and Coauthors predisposed to autosomal dominant Alzheimer disease (ADAD). In a cross-sectional study, Quiroz and coauthors used positron emission tomography imaging to measure amyloid and Clinical Review & Education tau deposition in 24 participants (mean [SD] age, 38.0 [7.4] years) from a large Colombian Review kindred with ADAD. The authors report that amyloid accumulates in the cortex of unim- paired presenilin 1 E280A mutation carriers 10 to 15 years before symptom onset, whereas tau deposits emerge in the medial temporal lobe approximately 6 years before and then spread into the cortex as carriers move closer to clinical onset. These findings suggest that amyloid prompts the spread of tau pathology beyond the medial temporal lobe and that the presence of tau is closely associated with memory decline. Editorial perspective is pro- vided by McDade and Bateman. Editorial 536 Risk of Serotonin Syndrome With Triptans and Antidepressants 566 In 2006, the US Food and Drug Administration issued a warning regarding the potential risk of serotonin syndrome with coprescription of triptan antimigraine drugs and selective sero- 620 Review of the Neurological toninreuptakeinhibitororselectivenorepinephrinereuptakeinhibitorantidepressantsbased Implications of von Hippel–Lindau Disease D Dornbos III and Coauthors on a small number of case reports.
    [Show full text]
  • Catatonia, Serotonin Syndrome and Parkinsonism
    MJP Online Early 01-01-17 CASE REPORT A Diagnostic Dilemma: Catatonia, Serotonin Syndrome and Parkinsonism Mohd Miharbei MF1,2, Ahmad Zafri AB1, Suhaila MZ1 1Jabatan Psikiatri dan Kesihatan Mental, Hospital Tengku Ampuan Afzan, 25100 Kuantan, Pahang, Malaysia 2Department of Psychological Medicine, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia Abstract Catatonia may concomitantly occur with other psychiatric diagnoses such as Major Depressive Disorder, however problem in diagnosis may arise due to the overlapping features with other problems such as serotonin syndromes, neuroleptic malignant syndromes and Parkinsonism. Despite the diagnostic dilemma and lack of diagnostic tools, the clinical correlation between the carbon monoxide poisoning and the late-onset development of the Parkinsonian features is the highlight of this report. Keywords: Catatonia, Parkinsonism, Carbon Monoxide Poisoning Introduction symptoms such as stuporous nature of the patient, rigidity, tremor and bradykinesia. Catatonic syndromes are a diagnostic conundrum and always offer a therapeutic Despite the similarity, the option and challenge as well. Catatonia is an associated response towards treatment are quite feature in major psychiatric diagnoses, as different. While electroconvulsive therapy is well as a prominent overlapping features in a known treatment option in catatonic state, neuroleptic malignant syndrome, akinetic it may not be the case for the state of parkinsonism and representing motor serotonergic syndrome and Parkinsonism. features of serotonergic syndromes [1,3]. The list of the possible cause of similar Case report presentations are vast. Among others, carbon monoxide poisoning is known to Mr LHC, a 58 years old Chinese male, with cause delayed onset Parkinsonism [2]. background history of methamphetamine abuse, presented to the hospital following Among the said differentials, there are few unconsciousness episode at home.
    [Show full text]
  • Serotonin Syndrome in Stroke Patients
    J Rehabil Med 2015; 47: 282–285 CASE REPORT Serotonin SYNDROME IN STROKE patients Sung Ho Jang, MD1*, Yong Min Kwon, MD1* and Min Cheol Chang, MD2 From the 1Department of Physical Medicine and Rehabilitation, College of Medicine, Yeungnam University and 2Department of Physical Medicine and Rehabilitation, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea. *These authors contributed equally to this study. Objective: Serotonin syndrome is a potentially life-threaten- Dopaminergic agents are known to be effective in improve- ing condition that can be caused by administration of agents ment of cognitive, language, motor, and executive function that increase serotonergic activity in the brain. We report in stroke patients (3). Therefore, dopaminergic drugs are here on 2 stroke patients who presented with serotonin syn- often prescribed for stroke patients during rehabilitation; drome following administration of dopaminergic agents. however, administration of dopaminergic drugs is associated Case report: Two stroke patients were administered ropin- with the risk of inducing SS (1, 4, 5). Although SS has been irole (patient 1) and carbidopa/levodopa (patient 2) during reported in other brain pathologies, including depressive rehabilitation. Both patients exhibited the clinical features of disorder and Parkinson’s disease, little is known about SS in serotonin syndrome, coinciding with an increase in dosage of stroke patients (5). each drug. Based on the clinical features included in revised We report here on 2 stroke patients who presented with SS Radomski’s criteria, they presented with 3 major symptoms after administration of dopaminergic agents. with 3 and 2 minor symptoms, respectively. The drugs that were thought to trigger serotonin syndrome were discontin- ued and the patients underwent conservative treatment.
    [Show full text]
  • Diagnosis of Serotonin Syndrome in the Intensive Care Population: a Case Report
    Netherlands Journal of Critical Care Accepted December 2013 CASE REPORT Diagnosis of serotonin syndrome in the intensive care population: a case report X. Zuidema1, I. Wilting2, M. Kromkamp3, J. Kesecioglu1 1Department of Intensive Care Medicine, Division of Anesthesiology, Intensive Care and Emergency Medicine Department of Intensive Care Medicine, University Medical Center Utrecht, the Netherlands 2Department of Clinical Pharmacy, Division Laboratory and Pharmacy, University Medical Center Utrecht, the Netherlands 3Department of Psychiatry, University Medical Center Utrecht, the Netherlands Correspondence X. Zuidema – e-mail: [email protected] Keywords – Serotonin syndrome, ICU, diagnosis Abstract by rapid treatment, however, is crucial, since a significant ICU admission due to serotonin syndrome (SS) is well proportion of SS cases (17%) lead to a worse outcome, with a described in the literature. However, development of SS during mortality rate of up to 0.2%.3 SS is mostly seen as a result of ICU admission has not been reported to date. We present a inadvertent interactions between serotonin-active drugs and/ patient in whom SS was suspected during ICU admission. or intentional self-poisoning.4,5 We describe a patient who was SS may be induced by either increased serotonergic activity suspected of SS during ICU admission, whilst continuing a or by lowering the cerebral serotonin sensitivity threshold. medication regime that included citalopram and amitriptyline. SS is not easily recognized, especially in ICU populations because it can easily be confused with clinical deterioration Case report or other drug-related toxidromes. SS is a potentially fatal A fifty-five year old somnolent male was admitted to the clinical syndrome, which requires rapid diagnosis and timely Department of Internal Medicine of a large academic teaching treatment.
    [Show full text]
  • Movement Disorders Emergencies Part 1 Hypokinetic Disorders
    NEUROLOGICAL REVIEW SECTION EDITOR: DAVID E. PLEASURE, MD Movement Disorders Emergencies Part 1 Hypokinetic Disorders Bradley J. Robottom, MD; William J. Weiner, MD; Stewart A. Factor, DO ovement disorders usually do not require emergent intervention; nevertheless, there are acute/subacute clinical settings in which the neurologist is consulted. It is in these circumstances that the neurologist must be prepared to accurately diagnose and properly treat the patient. We have reviewed the literature regarding move- Mment disorder emergencies and divided them into hypokinetic (part 1) and hyperkinetic (part 2) presentations. In part 1, drug-induced syndromes including neuroleptic malignant syndrome, par- kinsonism hyperpyrexia syndrome, and serotonin syndrome will be discussed. Emergency com- plications related to the management of Parkinson disease, including falling, motor fluctuations, and psychiatric issues, will also be reviewed. Arch Neurol. 2011;68(5):567-572 Movement disorders often have an insidi- DRUG-INDUCED MOVEMENT ous onset and slow progression and are not DISORDER EMERGENCIES often associated with emergency situa- tions. However, neurologists may be called Neuroleptic Malignant Syndrome on to diagnose and treat evolving move- ment disorders or acute complications of Neuroleptic malignant syndrome, first de- existing diseases in the emergency depart- scribed in 1960,2 is an iatrogenic disorder re- ment or intensive care unit. Such situa- sulting from exposure to drugs that block tions meet the working definition of an dopamine
    [Show full text]
  • Serotonin Syndrome in Asymptomatic Huntington's Disease
    Serotonin syndrome I Case notes Serotonin syndrome in asymptomatic Huntington’s disease Verity Haffenden BSc, MBBS, Anish Patel MBChB, MRCPsych, MedEd(Cert) Serotonin syndrome is a rare Figure 1. Hunter’s Criteria (adapted from Boyer and Shannon, 2005)6 and serious condition most often resulting from iatrogenic insult; the prescriber’s pen is Has a serotonergic agent been administered in the past five weeks? sometimes the most poisonous. Here, Dr Haffenden and Dr No Yes Patel discuss a complex case of serotonin syndrome in a patient with genetically proven, but not Not serotonin Are any of the following symptoms yet symptomatic, Huntington’s syndrome present? disease and chronic renal Tremor and hyperreflexia impairment. A screening Spontaneous clonus process is proposed to recognise the multitude of No Muscle rigidity, temperature >38°C, and Yes precipitating factors, which either ocular clonus or inducible clonus aligned in this case, and could Ocular clonus and either agitation or either alter our prescribing or diaphoresis expedite recognition. Inducible clonus and either agitation or diaphoresis untington’s disease (HD), a Hprogressive neurodegenerative Not serotonin Serotonin disease, is clinically diagnosed with syndrome syndrome a triad of signs/symptoms: chorea; psychiatric illness, and dementia. Research has shown neurotransmit- surgery was performed using a Past medical history of note ter deficits in mice models of Hun- cadaveric specimen but his postoper- included a genetic, but not yet tington’s1 both before and after ative period was complicated by anti- symptomatic, diagnosis of HD and symptomatic disease presence2 – body-mediated rejection and past psychiatric history included namely a reduction in serotonin.
    [Show full text]