Bulbar Palsy, Progressive
Serotonin Syndrome
Serotonin Uptake Inhibitors
Serotonin
Monoamine Oxidase Inhibitors
Encyclopedias as Topic
Adrenergic Uptake Inhibitors
Antiganglioside antibody in patients with Guillain-Barre syndrome who show bulbar palsy as an initial symptom. (1/48)
OBJECTIVES: To identify valuable antiganglioside antibodies that support the diagnosis of Guillain-Barre syndrome (GBS) and its variants in patients showing bulbar palsy as an initial symptom. METHODS: Medical records of 602 patients with GBS or its variants were reviewed. Fifteen patients had bulbar palsy as an initial symptom. Serum antibodies against GM1, GM1b, GD1a, GalNAc-GD1a, GT1a, and GQ1b were examined in 13 of them. RESULTS: Serum antiganglioside antibodies were positive in 11 (85%) patients. IgG anti-GT1a (n=8; 62%) and anti-GM1b (n=7; 54%) antibodies were often present, whereas all the patients had low or no anti-GM1 antibody activity. High anti-GD1a and anti-GQ1b IgG antibody titres were also present in some patients, but most had higher IgG antibody titres to GM1b or GT1a. All five patients with high IgG antibody titre to GM1b or GT1a only had had antecedent diarrhoea. Some patients with pharyngeal-cervical-brachial weakness (PCB) had IgG antibody to GT1a which did not cross react with GQ1b. Other patients with PCB had antibody to GT1a which cross reacted with GQ1b or antibody to GM1b, but anti-GM1b and anti-GT1a antibodies were not associated with the presence of bulbar palsy. All the patients who had no IgG antiganglioside antibodies recovered completely. CONCLUSIONS: Measurement of serum IgG anti-GT1a and anti-GM1b antibodies gives helpful support for the diagnosis of GBS and its variants when there is early involvement of the oropharyngeal function independently of other neurological findings which appear as the illness progresses. (+info)Worster-Drought syndrome, a mild tetraplegic perisylvian cerebral palsy. Review of 47 cases. (2/48)
A retrospective case-note analysis was undertaken of 47 children with a congenital upper motor neurone bulbar palsy (excluding pure speech dyspraxia) to clarify the phenotype of Worster-Drought syndrome (WDS) and to record its associated features and complications. The results revealed that the study children had significant bulbar problems (with 80% still needing a modified diet and a similar number using augmentative communication methods at last review). There were also high rates of predictable bulbar complications (86% had dribbling, 60% had glue ear, gastro-oesophageal reflux in 40%, history of poor nutrition in 40% and aspiration in 40%). Most of the children had additional complex impairments (91% had mild pyramidal tetraplegia, 81% learning difficulties, 60% congenital defects, 41% neuropsychiatric problems and 28% epilepsy). Over half of the children had significant medical problems in the first year, but mean age at diagnosis was 6 years. There were no obvious causes in pregnancy or birth. Six children had a family history of WDS and 32% (12/37) had abnormal neuroimaging including five with bilateral perisylvian polymicrogyria. In our experience, WDS is not uncommon, is relatively easily diagnosed and is crucial not to miss as the management of these children's multiple impairments is complex and requires a careful team approach. WDS falls clearly within the cerebral palsies as a syndrome that includes motor impairment arising from static damage to the brain in early life. The common presence of cognitive, behavioural and seizure impairments strongly supports the cerebral cortical (presumably perisylvian) localization. Its core elements are a suprabulbar paresis, a mild spastic tetraplegia and a significant excess of cognitive and behavioural impairments and epilepsy. The complete overlap in phenotype between WDS and the bilateral perisylvian syndrome leads us to propose that they are the same condition. WDS is startlingly absent from epidemiological studies of the cerebral palsies and rarely diagnosed, presumably because of lack of clinical awareness of the condition and lack of major gross motor impairments. (+info)Motor neuron diseases in the university hospital of Fortaleza (Northeastern Brazil): a clinico-demographic analysis of 87 cases. (3/48)
In this retrospective (1980-1998) study, we have analyzed clinico-demographically, from the records of the University Hospital of Fortaleza (Brazil), a group of 87 patients showing signs and symptoms of motor neuron diseases (MNDs). Their diagnosis was determined clinically and laboratorially. The WFN criteria were used for amyotrophic lateral sclerosis (ALS) diagnosis. The clinico-demographic analysis of the 87 cases of MNDs showed that 4 were diagnosed as spinal muscular atrophy (SMA), 5 cases as ALS subsets: 2 as progressive bulbar paralysis (PBP), 2 as progressive muscular atrophy (PMA) and 1 as monomelic amyotrophy (MA), and 78 cases of ALS. The latter comprised 51 males and 27 females, with a mean age of 42.02 years. They were sub-divided into 4 groups according to age: from 15 to 29 years (n= 17), 30 to 39 years (n= 18), 40 to 69 years (n= 39) and 70 to 78 years (n= 4). From the 78 ALS patients, 76 were of the classic sporadic form whilst only 2 were of the familial form. The analysis of the 87 patients with MNDs from the University Hospital of Fortaleza showed a predominance of ALS patients, with a high number of cases of juvenile and early onset adult sporadic ALS. (+info)Non-invasive screening for surgical intracranial lesions. (4/48)
The value and reliability of the combined results of skull radiographs, electroencephalography, echoencephalography, isotope angiography, and brain scanning in 147 patients suspected of having an intracranial space occupying lesions are analysed. The overall accuracy of the technique was 79%. No false negatives were found. The advantages of adopting the system proposed by the authors in everyday clinical work is discussed. (+info)Rehabilitation for postpolio sequelae. (5/48)
BACKGROUND: Postpolio sequelae (PPS) are new, late manifestations that occur many years after the initial poliomyelitis infection. Recurrence of symptoms and fear of reactivation of the polio virus is particularly distressing to polio survivors. OBJECTIVE: This article outlines the diagnosis, pathophysiology, and management of PPS disabilities using a case vignette. DISCUSSION: Clinical features of PPS include fatigue, joint and muscle pain, new muscular weakness and bulbar symptoms. Diagnosis can be complicated particularly in nonparalytic cases of poliomyelitis. Disabilities in PPS may not be obvious to the observer but significantly affect the quality of life of the PPS patient. Previous rehabilitation intervention focussed on physical effort and determination to overcome disability at all costs. The treatment in PPS is now modified, and aggressive physical measures that may exacerbate muscle weakness are avoided. Most disabilities in PPS can be well managed with rehabilitation interventions that address limitations in patient activities of daily living, mobility and cardiopulmonary fitness. (+info)Subacute bulbar palsy as the initial sign of follicular thyroid cancer. (6/48)
We report a 64-year-old woman with follicular thyroid cancer found by subacute bulbar palsy. Progressive bulbar palsy (PBP) was considered the most likely diagnosis, because no abnormal finding was detected on brain CT and blood test except for the decrease of free T4. An echogram of the thyroid revealed a small nodule which was shown to be class IIb by fine needle biopsy. However, 201Tl scintillation examination showed skull base metastasis. Follicular thyroid cancer sometimes seems to manifest as a distant metastasis with no clinically evident thyroid lesion. This case suggested the importance of a detailed survey for malignancy, when subacute bulbar palsy is seen. (+info)Congenital oculo-bulbar palsy. (7/48)
A girl developed progressive weakness of bulbar and ocular muscles starting before the age of two years. Electromyography revealed a widespread subclinical myopathy. An intercostal muscle biopsy showed complex abnormalities including occasional neurofilamentous accumulations and honeycomb-like membranous material in terminal axons. Endplates were small and some secondary synaptic clefts were abnormally deep. Acetylcholine receptors extended unusually deeply into the clefts of the junctional folds. Muscle fibres showed subsarcolemmal vacuolation at some places. This form of congenital oculo-bulbar palsy does not appear to have been described previously. (+info)The Scottish Motor Neuron Disease Register: a prospective study of adult onset motor neuron disease in Scotland. Methodology, demography and clinical features of incident cases in 1989. (8/48)
The Scottish Motor Neuron Disease Register (SMNDR) is a prospective, collaborative, population based study of motor neuron disease (MND) in Scotland. The register started in January 1989 with the aim of studying the clinical and epidemiological features of MND by prospectively identifying incident patients. It is based on a system of registration by recruitment from multiple sources, followed by the collection of complete clinical data and follow up, mainly through general practitioners. In this report the register's methodology and the demography and incidence data for the first year of study are presented. One hundred and fourteen newly diagnosed patients were identified in 1989 giving a crude incidence for Scotland of 2.24/100,000/year. Standardised incidence ratios showed a non-significant trend towards lower rates in north eastern regions and island areas. (+info)Progressive bulbar palsy (PBP) is a form of motor neuron disease (MND), also known as Amyotrophic Lateral Sclerosis (ALS). It is characterized by the progressive degeneration of the motor neurons in the brainstem, which control vital functions such as swallowing, speaking, chewing, and breathing.
In PBP, these symptoms gradually worsen over time, often resulting in severe disability and ultimately death due to respiratory failure. The progression of the disease can vary from person to person, but it typically advances more slowly than other forms of ALS. There is currently no cure for PBP or any other form of MND, and treatment is focused on managing symptoms and maintaining quality of life.
Serotonin syndrome is a potentially life-threatening condition that arises from excessive serotonergic activity in the central nervous system (CNS) and peripheral nervous system. It is typically caused by the interaction of medications, illicit substances, or dietary supplements that increase serotonin levels or enhance serotonin receptor sensitivity.
The diagnostic criteria for serotonin syndrome include:
1. Presence of a serotonergic medication or drug known to cause the syndrome
2. Development of neuromuscular abnormalities, such as hyperreflexia, myoclonus, tremor, rigidity, or akathisia
3. Autonomic dysfunction, including diaphoresis, tachycardia, hypertension, dilated pupils, and hyperthermia
4. Mental status changes, such as agitation, confusion, hallucinations, or coma
5. Symptoms that develop rapidly, usually within hours of a change in serotonergic medication or dosage
Serotonin syndrome can range from mild to severe, with the most severe cases potentially leading to respiratory failure, rhabdomyolysis, disseminated intravascular coagulation (DIC), and death. Treatment typically involves discontinuation of the offending agent(s), supportive care, and pharmacologic interventions such as cyproheptadine or cooling measures for hyperthermia.
Methylergonovine is a medication that belongs to a class of drugs called ergot alkaloids. It is primarily used to prevent and treat uterine bleeding after childbirth. Medically, it is defined as a semi-synthetic ergopeptide analog with oxytocic properties, which stimulates myometrial contractions and reduces postpartum hemorrhage.
Methylergonovine works by stimulating the smooth muscle of the uterus, causing it to contract. This helps to return the uterus to its pre-pregnancy size and also helps to control bleeding after childbirth. It is important to note that methylergonovine should only be used under the supervision of a healthcare provider, as it can have serious side effects if not used properly.
Serotonin uptake inhibitors (also known as Selective Serotonin Reuptake Inhibitors or SSRIs) are a class of medications primarily used to treat depression and anxiety disorders. They work by increasing the levels of serotonin, a neurotransmitter in the brain that helps regulate mood, appetite, and sleep, among other functions.
SSRIs block the reuptake of serotonin into the presynaptic neuron, allowing more serotonin to be available in the synapse (the space between two neurons) for binding to postsynaptic receptors. This results in increased serotonergic neurotransmission and improved mood regulation.
Examples of SSRIs include fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), citalopram (Celexa), and escitalopram (Lexapro). These medications are generally well-tolerated, with side effects that may include nausea, headache, insomnia, sexual dysfunction, and increased anxiety or agitation. However, they can have serious interactions with other medications, so it is important to inform your healthcare provider of all medications you are taking before starting an SSRI.
Serotonin, also known as 5-hydroxytryptamine (5-HT), is a monoamine neurotransmitter that is found primarily in the gastrointestinal (GI) tract, blood platelets, and the central nervous system (CNS) of humans and other animals. It is produced by the conversion of the amino acid tryptophan to 5-hydroxytryptophan (5-HTP), and then to serotonin.
In the CNS, serotonin plays a role in regulating mood, appetite, sleep, memory, learning, and behavior, among other functions. It also acts as a vasoconstrictor, helping to regulate blood flow and blood pressure. In the GI tract, it is involved in peristalsis, the contraction and relaxation of muscles that moves food through the digestive system.
Serotonin is synthesized and stored in serotonergic neurons, which are nerve cells that use serotonin as their primary neurotransmitter. These neurons are found throughout the brain and spinal cord, and they communicate with other neurons by releasing serotonin into the synapse, the small gap between two neurons.
Abnormal levels of serotonin have been linked to a variety of disorders, including depression, anxiety, schizophrenia, and migraines. Medications that affect serotonin levels, such as selective serotonin reuptake inhibitors (SSRIs), are commonly used to treat these conditions.
Monoamine oxidase inhibitors (MAOIs) are a class of drugs that work by blocking the action of monoamine oxidase, an enzyme found in the brain and other organs of the body. This enzyme is responsible for breaking down certain neurotransmitters, such as serotonin, dopamine, and norepinephrine, which are chemicals that transmit signals in the brain.
By inhibiting the action of monoamine oxidase, MAOIs increase the levels of these neurotransmitters in the brain, which can help to alleviate symptoms of depression and other mood disorders. However, MAOIs also affect other chemicals in the body, including tyramine, a substance found in some foods and beverages, as well as certain medications. As a result, MAOIs can have serious side effects and interactions with other substances, making them a less commonly prescribed class of antidepressants than other types of drugs.
MAOIs are typically used as a last resort when other treatments for depression have failed, due to their potential for dangerous interactions and side effects. They require careful monitoring and dosage adjustment by a healthcare provider, and patients must follow strict dietary restrictions while taking them.
An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.
Adrenergic uptake inhibitors are a class of medications that work by blocking the reuptake of neurotransmitters, such as norepinephrine and dopamine, into the presynaptic neuron. This results in an increase in the amount of neurotransmitter available to bind to postsynaptic receptors, leading to an enhancement of adrenergic transmission.
These medications are used in the treatment of various medical conditions, including depression, attention deficit hyperactivity disorder (ADHD), and narcolepsy. Some examples of adrenergic uptake inhibitors include:
* Tricyclic antidepressants (TCAs): These medications, such as imipramine and amitriptyline, were developed in the 1950s and are used to treat depression, anxiety disorders, and chronic pain.
* Selective serotonin-norepinephrine reuptake inhibitors (SNRIs): These medications, such as venlafaxine and duloxetine, were developed in the 1990s and are used to treat depression, anxiety disorders, and chronic pain.
* Norepinephrine-dopamine reuptake inhibitors (NDRIs): These medications, such as bupropion, are used to treat depression and ADHD.
It's important to note that these medications can have side effects and should be used under the supervision of a healthcare provider.
Progressive bulbar palsy
Pathology of Motor Neuron Disorders: Definition, Etiology, Epidemiology
Article - Billing and Coding: Swallowing Studies for Dysphagia (A56621)
Voice and Swallowing Center | UCSF Health
FAQs | Amyotrophic Lateral Sclerosis (ALS) | CDC
Dr. Stephen Scelsa, MD, Neurology Specialist - New York, NY | Sharecare
walker | ALS Support Community
Online ICD9/ICD9CM codes
ALS and MND: Symptoms, causes, treatment
Amyotrophic Lateral Sclerosis (ALS) and Other Motor Neuron Diseases (MNDs) - Neurologic Disorders - MSD Manual Professional...
Obituaries - Daily Bulldog - Page 680
The varied motor neuron disease phenotypes | ACNR Journal
Potential physiotherapy practice - nmmra.org
DeCS - Changed terms