A 77-year-old man presented with bilateral choreic movements that had developed over the past month. He had a history of poorly controlled type 2 diabetes. At admission, he was found to have severe hyperglycemia without ketosis. A CT scan showed hyperdensity in the putamen and lenticular nucleus. Treatment with insulin, haloperidol, and glycemic control led to regression of the choreic movements within 4 days. Chorea secondary to nonketotic hyperglycemia is a rare complication of uncontrolled diabetes that is usually reversible with normalization of blood glucose levels and neuroleptic treatment. The pathophysiology is thought to involve metabolic disturbances from hyperglycemia impairing neurotransmission in basal ganglia structures and
Intra-Fetal Laser Ablation of Umbilical Vessels in Acardiac Twin with Success...Apollo Hospitals
To interrupt blood supply to the acardiac twin in a case of TRAP sequence of monochorionic diamniotic multiple pregnancy to allow for continuation of the normal twin.
Intra-Fetal Laser Ablation of Umbilical Vessels in Acardiac Twin with Success...Apollo Hospitals
To interrupt blood supply to the acardiac twin in a case of TRAP sequence of monochorionic diamniotic multiple pregnancy to allow for continuation of the normal twin.
Hematoma expansion after spontaneous intracerebral hemorrhageWafik Bahnasy
The size of the hematoma grows due to rebleeding in the next few hours after the onset in up to 40% of cases which results in early neurological deterioration, poor functional outcome and increased mortality.
Review of a rare but important cardiac dysplasia causing high mortality and morbidity in mostly young patients.
In this presentation, the epidemiology, pathophysiology, diagnosis and treatment of said disease is examines.
Movement disorders: A complication of chronic Hyperglycemia? A case reportApollo Hospitals
The association of chorea with a specific lesion on brain imaging is described as an atypical manifestation of chronic hyperglycemia. This is a rare syndrome, affecting more elderly, presenting a diabetes poorly controlled. There is hyperglycemia without ketosis and moderate hyperosmolarity.
Hematoma expansion after spontaneous intracerebral hemorrhageWafik Bahnasy
The size of the hematoma grows due to rebleeding in the next few hours after the onset in up to 40% of cases which results in early neurological deterioration, poor functional outcome and increased mortality.
Review of a rare but important cardiac dysplasia causing high mortality and morbidity in mostly young patients.
In this presentation, the epidemiology, pathophysiology, diagnosis and treatment of said disease is examines.
Movement disorders: A complication of chronic Hyperglycemia? A case reportApollo Hospitals
The association of chorea with a specific lesion on brain imaging is described as an atypical manifestation of chronic hyperglycemia. This is a rare syndrome, affecting more elderly, presenting a diabetes poorly controlled. There is hyperglycemia without ketosis and moderate hyperosmolarity.
ASSESSMENT AND PLANNING GUIDE FOR USE IN THE HOSPITALThe followi.docxgalerussel59292
ASSESSMENT AND PLANNING GUIDE FOR USE IN THE HOSPITAL
The following information should be included daily as it applies to your patient.
Demographic DataDate of AdmissionVital Signs
39 y/o African American male
10/28/18
BP: 115/60. Pain: 2
P: 91
T: 98.2.
RR: 22
SP02: 95
Significant Past Medical HistoryAllergies/Reactions
HTN, Hyperlipemia, Diabetes
NKA
Reason for Hospitalization and Current Diagnosis
Current Diagnosis: Acute Embolic Stroke, Cerebral Edema, R Hemiparesis, Pneumonia
Reason for hospitalization: 38 y/o male with a history of HTN presented with onset Right Sided Weakness and confusion at 11pm on 10-27-18 when he went to sleep. He woke up at 3am and he was talking gibberish to his fiancé. He went back to sleep and 2 hours later his symptoms had worsened. On 10-28-18, EMS was called by his fiancé and he was taken to the ER. His fiancé said he had taken “something” possibly cocaine. Patient was diagnosed with Acute Embolic Stroke, Cerebral Edema, R Hemiparesis and recently Pnuemonia.
Describe thepathophysiologyincluding signs, symptoms and incidence; and compare with patient findings:
· Acute Embolic Stroke:
Pathophysiology: Occurs when a blood clot that forms somewhere elsewhere in the body breaks loose and then travels to the brain through the bloodstream. The clot can lodge in an artery and blocks the flow of blood.
Common symptoms:Difficulty speaking or understanding words, numbness and tingling, temporary paralysis, blurred vision or blindness, slurred speech, dizziness, feeling faint, difficulty swallowing, nausea, sleepiness. Embolic stroke doesn’t cause any unique symptoms
Muscular symptoms: Difficulty with coordination, stiff muscles, feelings of weakness on one side or all of the body.
Cognitive symptoms: Mental confusion, an altered level of consciousness, visual agnosia
Patient Findings: Patient presented with R hemiparesis, facial drooping, slurred speech, difficulty swallowing.
· Cerebral Edema
Pathophysiology: It’s a life threatening condition that causes fluid to develop in the brain.
This fluid increases the pressure inside of the skull causing intracranial pressure (ICP). Increased ICP can reduce brain blood flow and decrease the oxygen your brain receives. The brain needs an uninterrupted flow of oxygen to function properly.
Symptoms: Headache, dizziness, nausea, lack of coordination, numbness, mood changes, memory loss, difficulty speaking, incontinence, change in consciousness, seizures, weakness in extremities
Patient Findings: Patient presented with difficulty speaking, incontinence, change in consciousness, weakness in extremities
· Hemiparesis
Pathophysiology: Hemiparesis is weakness on one side of the body. One side can still move but with reduced muscular strength.
Symptoms: Difficulty walking, standing, and maintaining your balance. You may also have numbness or tingling on your weaker side.
Patient findings: Patient has right sided weakness.
· Pneumonia
.
Diabetic ketoacidosis induced cerebral infarct - A missing link in pathogenes...Apollo Hospitals
Diabetic ketoacidosis (DKA) is a known complication of acute pancreatitis (AP). We report a case of DKA precipitated by AP. This patient developed watershed infarct in brain during her course of disease which was possibly attributed to hypercoagulability, stasis and endothelial injury triggered by ketosis.
In a pregnant woman presenting with thrombocytopenia, the possibility of HELLP syndrome should always be considered by the treating clinician so as to initiate the therapy at the earliest to prevent the high perinatal mortality and postpartum morbidity. Here we report an unusual case of young Primigravida (postpartum) who presented at Indraprastha Apollo hospitals, New Delhi with altered sensorium, paraperesis, DIC and septic shock. On evaluation she was found to have HELLP syndrome for which Plasmapheresis was given and patient showed remarkable improvement.
IgA nephropathy is a condition characterized by deposition of IgA immunoglobulins in glomeruli. This condition is fairly common in Western countries. The scope of the disease is wide and case by case. Cases of IgA nephropathy are rare. Our case report is of a young man who developed rapid onset IgA nephropathy leading to end stage renal disease ESRD . This case report describes a 26 years age young man who presented and eventually presented with microscopic hematuria and severe proteinuria. Hemodialysis for his burned out IgA nephropathy. Dr. Thenmozhi. P | Yuvaraj. B "IgA Nephropathy (Burger's Disease): Case Report" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-7 | Issue-1 , February 2023, URL: https://www.ijtsrd.com/papers/ijtsrd52706.pdf Paper URL: https://www.ijtsrd.com/medicine/other/52706/iga-nephropathy-burgers-disease-case-report/dr-thenmozhi-p
Hypokalemia, Hypoxic Ischemic Encephalopathy, Nosocomial Pneumonia and Urinar...Jack Frost
Hypokalemia, Hypoxic Ischemic Encephalopathy, Nosocomial Pneumonia and Urinary Tract Infection. This presentation contains real names of persons involve of this particular study. This names should not be copied or rewritten. Used the data of this study as basis only. All rights reserved 2009.
Hypokalemia, Hypoxic Ischemic Encephalopathy, Nosocomial Pneumonia and Urinar...Jack Frost
Hypokalemia, Hypoxic Ischemic Encephalopathy, Nosocomial Pneumonia and Urinary Tract Infection.This presentation contains real names of persons involve of this particular study. This names should not be copied or rewritten. Used the data of this study as basis only. All rights reserved 2009.
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Malignant mixed mullerian tumors are very rare genital tumors. They are biphasic neoplasms composed of an admixture of malignant epithelial and mesenchymal elements. In descending order of frequency they originate in the uterus, ovaries, fallopian tubes, cervix and vagina. Also they arise denovo from peritoneum. They are highly aggressive and tend to occur in postmenopausal low parity women. Because of rarity, there is as such no treatment guidelines available. Multimodality treatment in the form of radical surgery followed by adjuvant chemotherapy or radiotherapy or combined chemoradiation gives a better prognosis & outcome. Two case reports of such tumors, one from ovary and other from penitoneum are presented along with the review of literature.
Breast Cancer in Young Women and its Impact on Reproductive FunctionApollo Hospitals
Breast cancer is the most common cancer in women in developed countries. Chemotherapy for breast cancer is likely to negatively impact on reproductive function. We review current treatment; effects on reproductive function; breastfeeding and management of menopausal symptoms following breast cancer.
Turner syndrome (gonadal dysgenesis) is one of the most common chromosomal abnormalities occuring 1 in 2500 to 1 in 3000 live-born girls. It is an important cause of short stature in girls and primary amenorrhea in young women that is usually caused by loss of part or all of an X chromosome. This review briefly summarises the current knowledge about the syndrome and the management strategies.
Due to pregnancy thyroid economy is affected with changes in iodine metabolism, TBG and development of maternal goiter. The incidence of hypothyroidism in pregnancy is quite common with autoimmune hypothyroidism being the most important cause. Overt as well as subclinical hypothyroidism has a varied impact on maternal and neonatal outcome. After multiple studies also, routine screening in pregnancy for hypothyroidism can still not be recommended. Management mainly comprises of dosage adjustments as soon as pregnancy is diagnosed based on results of thyroid function tests. The aim should be to keep FT4 at the upper end of normal range.
Growth Hormone Deficiency (GHD) can persist from childhood or be newly acquired. Confirmation through stimulation testing is usually required unless there is a proven genetic/structural lesion persistent from childhood. Growth harmone (GH) therapy offers benefits in body composition, exercise capacity, skeletal integrity, and quality of life measures and is most likely to benefit those patients who have more severe GHD. The risks of GH treatment are low. GH dosing regimens should be individualized. The final decision to treat adults with GHD requires thoughtful clinical judgment with a careful evaluation of the benefits and risks specific to the individual.
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Viral infections like HIV, hepatitis Band C virus pose a big risk to the contacts of individuals with high risk behaviour as well as to the attending health care workers. Blood, semen, vaginal and other potentially infectious materials can transmit the infection to the susceptible contacts. Universal precautions should be strictly implemented during clinical examination, laboratory work and surgical procedures to prevent transmission to the health care providers. Health care workers should receive vaccination for hepatitis B infection. An inadvertent exposure should be managed with proper first aid and infectivity of the source and severity of exposure should be assessed. Severity of exposure is based on the nature and area of exposed surface, mode of injury and volume of infective material. Post-exposure prophylaxis (PEP) should be started as soon as possible after a proper counseling about the effectiveness of post-exposure prophylaxis, side effects and risk of carrying the infection to his familial contacts and its prevention.
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Laparoscopic cholecystectomy has now become the treatment of choice for the gall bladder stone. With increasing experience, surgeon has started to take more difficult cases which were considered relative contra indications for laparoscopic removal of gall bladder few years back.
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
2. Case Report
Movement disorders: A complication of chronic
hyperglycemia? A case report
R. Ben Othman a,
*, A. Ben Mahmoud b
, A. Mankai a
, N. Trabelsi a
,
F. Hentati b
, F. Ben Mami a
a
Department (C) of Diabetology, Nutrition and Metabolic Diseases, The National Institute of Nutrition,
Avenue Jbel Lakhdhar, 1007 Tunis, Tunisia
b
Department of Neurology, National Institute Mongi Ben Hmida of Neurology, Tunis, Tunisia
a r t i c l e i n f o
Article history:
Received 29 March 2013
Accepted 9 October 2013
Available online xxx
Keywords:
Diabetes mellitus
Chorea
Dyskinesia
Hyperglycemia
Nonketotic hyperglycemia
a b s t r a c t
Introduction: The association of chorea with a specific lesion on brain imaging is described
as an atypical manifestation of chronic hyperglycemia.
Case report: Patient of 77 years, hospitalized for bilateral choreic movements predominant
on the right with dystonic movements, appeared a month ago.
At admission: Hyperglycemia at 2.4 g/L, without ketosis, a type 2 diabetes (HbA1c 17.3%) on
oral antidiabetic agents. CT scan shows hyperdensity of putamen and lenticular nucleus
that eliminates an ischemic attack. Evolution after glycemic reequilibration and treatment
by haloperidol is favorable, with regression of chorea.
Discussion: This is a rare syndrome, affecting more elderly, presenting a diabetes poorly
controlled. There is hyperglycemia without ketosis and moderate hyperosmolarity. The
symptoms usually regress after glycemic control and neuroleptic treatment (recurrence in 13%
of cases). The appearance of this syndrome seems to be related to the achievement of the
control system GABAergic of the basal ganglia leading to an excitation of the cerebral cortex,
causing involuntary movements. The etiopathogenic hypotheses advanced are multiple:
impairedstriatal neurotransmissionassociated with metabolic disturbancesof hyperglycemia,
dysfunction ofthe hematoencephalicbarrier and abnormalitiesofthe cerebralvascularization.
Conclusion: Chorea secondary to nonketotic hyperglycemia is a rare complication and little
known of type 2 diabetes. Transitional neuroleptic treatment and glycemic control make
the symptoms regress in most cases with the disappearance of the lesion imaging.
Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved.
1. Introduction
The uncontrolled diabetes can be responsible for different
neurological symptoms such as epileptic seizures and disor-
ders of consciousness. Transient chorea or ballism provoked
by an episode of nonketotic hyperglycemia has been reported
by numerous authors over the past couple of decades.1,2
In
this case, the choreiform movements have resolved within
days after normalization of blood glucose. In the vast majority
of cases, the chorea/ballism triggered by hyperglycemia has
* Corresponding author. Tel.: þ216 97291139.
E-mail address: benothmanr@gmail.com (R. Ben Othman).
Available online at www.sciencedirect.com
ScienceDirect
journal homepage: www.elsevier.com/locate/apme
a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1 e3
Please cite this article in press as: Ben Othman R, et al., Movement disorders: A complication of chronic hyperglycemia? A case
report, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apme.2013.10.006
0976-0016/$ e see front matter Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.apme.2013.10.006
3. been unilateral. Several recent reports have documented
characteristic brain imaging findings consisting of high den-
sity on computed tomography (CT) scans. We describe a case
of chorea developing subacutely during an episode of revers-
ible nonketotic hyperglycemia.
2. Observation
A patient, aged 77 years, followed for type II diabetes on oral
antidiabetic agents for three months and for hypertension
since two years, presents to the emergency for abnormal
movements of the upper limbs, the head and neck. These
movements are type of flexion-extension and rotation. They
are abrupt, irregular and of large amplitude, exaggerating to
emotion and disappearing during sleep.
There is no remarkable family history or a prior history of
dopamine antagonist or estrogen medication use and no his-
tory of rheumatic fever/Sydenham’s chorea.
At admission, the patient was conscious, afebrile and well
oriented in time and space. Neurological examination objec-
tify chorea in both upper limbs, the head and neck predomi-
nant at right without oral or lingual abnormal movements. In
addition, the review found hypotonia in all four limbs.
The remainder of the examination shows no motor or
sensory deficit, nor parkinsonism nor cerebellar nor cranial
disorder. A specialized neuropsychological examination did
not show significant cognitive disorders (mini-mental
state ¼ 28/30) except an alteration of executive functions
(frontal score ¼ 8/18). In addition, a psychomotor instability
was noted as well as irritability.
A cerebral CT scan was performed in emergency, which
objectified a spontaneous hyperdensity of putamen and
lenticular nuclei (Fig. 1a et b). Our patient did not benefit of
brain MRI. Urinalysis was strongly positive for glucose and
negative for ketones. The following laboratory data were
notable: fasting blood glucose 13.2 mmol/l (240 mg/dl), glyco-
sylated hemoglobin A1c 17.3%, creatinine 140 mmol/l, clear-
ance 37 ml/min.
The patient was put on insulin and small doses of halo-
peridol (3 mg/day in three divided doses). A significant
reduction in abnormal movements was noted, these dis-
appeared within four days, which motivated progressive
stopping of haloperidol .The patient was admitted in dia-
betology for initiation of insulin 6UI at morning due to
contraindication for the use of oral antidiabetic .The patient is
still asymptomatic after six months. Control brain CT scan
was not performed.
3. Discussions
Chorea and ballism are hyperkinetic movement disorders
which are characterized by the occurrence of uncontrollable,
sudden, irregular, high amplitude and short duration move-
ments of all or a part of the body.3,4
Chorea and/or ballism have
been reported for the first time, as a complication of nonketotic
hyperglycemia by Bedwell in 1960.5
These abnormal move-
ments are rarely revealing of diabetes.2
The symptomatology is
made from hemichorea and/or hemiballismus in most cases
correlated to unilateral scannographic images.6
For our case
the damage is bilateral predominantly to the right in relation to
imagery and in accordance with some similar cases reported in
the literature where the lesion is bilateral.7
Physiopathology subtending the development of these
movements during hyperglycemia without ketosis is still un-
clear.3
Several hypotheses have been evoked.
Brain structures implicated in the genesis of chorea are
represented by the basal ganglia, mainly the subthalamic
nucleus, the way pallido-subthalamic, striatum and to a lesser
degree the cerebral cortex and the thalamus.8
These cores are
susceptible to ATP and cellular energy depletion which prob-
ably explain the predilection of lesions at their level.8
Indeed, during hyperglycemia, there is an alteration of the
bloodebrain barrier (BBB) leading to, on one hand, the reduc-
tion of regional cerebral blood flow and on the other hand, the
passage of the cerebral metabolism to anaerobic, resulting in
an inhibition of the tricarboxylic acid cycle (Krebs).9,10
Fig. 1 e (a and b) A CT scan showing a spontaneous hyperdensity in the putamen and the lenticular nucleus.
a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1 e32
Please cite this article in press as: Ben Othman R, et al., Movement disorders: A complication of chronic hyperglycemia? A case
report, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apme.2013.10.006
4. The brain then uses the gamma-aminobutyricacid (GABA) as
an alternative source of energy. In patients without ketosis,9e12
the amount of GABA and acetate is rapidly depleted.11,13
Because of this deficiency of acetate, acetylcholine synthesis
may also be decreased. The depletion of these two principal
neurotransmitters(GABAandacetylcholine) inthebasalganglia,
in combination with loss of energy and metabolic acidosis is the
cause of the appearance of movement disorders.11,13,14
Hyperglycemia has also a role in the extravasation of red
blood cells that is the cause of hemorrhagic suffusions found
in cerebral imaging of the majority of these patients.8
Other indirect factors have been incriminated in the genesis
of chorea, in fact most cases of chorea during nonketotic hy-
perglycemia have been reported in elderly patients with hy-
pertension associated with diabetes.14,15
Indeed, these two
vascular risk factors are often responsible for cerebral vascular
lesions especially lacunar mainly at the basal ganglia.16
These
lesions are usually not visible on standard neuroimagery, but
responsible for clinical manifestations such as chorea.14,17
Finally, the acanthocytosis as a predictor of the onset of
chorea during diabetes has been reported.12
Several hypotheses
have suggested that erythrocyte membrane proteins can un-
dergo, secondary to a particular metabolic state (diabetes),
functional and morphological changes, with acanthocytes for-
mation.18
So hyperviscosity induced by hyperglycemia may
cause a transient malfunction in striatal neurons in predisposed
individuals. This hypothesis is in agreement with the concept
that hyperglycemia worsens the evolution of stroke. For our
patient, the search for acanthocytes came back negative.
Chorea in the context of hyperglycemia without ketosis is
generally good prognosis. Most patients improve when
normalization of blood glucose, sometimes without the use of
neuroleptics or with very low doses.10,14
Radiological abnor-
malities may persist longer and disappear for days or weeks
after normalization of glycemia.12
Neuroleptics is the treatment of choice. Benzodiazepines
can also be used.
4. Conclusion
Chorea during uncontrolled diabetes is an unusual compli-
cation, however it remains favorable prognosis in most cases,
which makes necessary the knowledge of this association
since therapeutic implications arising.
Conflicts of interest
All authors have none to declare.
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a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1 e3 3
Please cite this article in press as: Ben Othman R, et al., Movement disorders: A complication of chronic hyperglycemia? A case
report, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apme.2013.10.006