Akathisia, Drug-Induced
Psychomotor Agitation
Dyskinesia, Drug-Induced
Antipsychotic Agents
Basal Ganglia Diseases
Parkinson Disease, Secondary
Diphenhydramine
Affective Disorders, Psychotic
Dibenzothiazepines
Benzodiazepines
Movement Disorders
Cholinergic Antagonists
Schizophrenia
Effect of leaf essential oil from Piper solmsianum C.DC. in mice behaviour. (1/63)
The essential oil from Piper solmsianum leaves and its major compound (sarisan) were tested to verify their influences upon mice behaviour. The essential oil was obtained by hydrodistillation in a modified Clevenger extractor and analysed by GC/ MS. This analysis revealed in the oil the presence of monoterpenes, sesquiterpenes and of arylpropanoids. The compound sarisan, a myristicin analogue, was isolated from the oil to perform the pharmacological tests. Emulsions of the oil and of sarisan (5.0 and 10.0% v/v) were used in the tests. Pentobarbital (30 mg/ kg s.c.) or diazepam (2.5 mg/ kg s.c.) were tested as standard drugs to verify depressant or anxiolytic effects, respectively. Both essential oil and sarisan showed to have exciting and depressant effects in the tested animals. (+info)The ability of environmental context to facilitate psychomotor sensitization to amphetamine can be dissociated from its effect on acute drug responsiveness and on conditioned responding. (2/63)
Doses of amphetamine or cocaine that fail to induce psychomotor sensitization when given to a rat in its home cage can produce robust sensitization if given immediately following placement into a relatively novel, distinct environment. A drug-associated context can serve as a conditioned stimulus, and therefore may promote robust sensitization by facilitating associative learning processes. We examined this hypothesis by habituating rats to the test environment for 1 or 6--8 hr prior to each drug injection, which degrades the ability of environmental context to serve as an effective conditioned stimulus. When 0.5 mg/kg of amphetamine was administered intravenously immediately after placement into a distinct environment there was a large acute psychomotor response (rotational behavior) on the first test day, and robust sensitization developed with repeated daily injections. When the same treatment was administered in the home cage, there was a small acute response and no sensitization developed. The enhanced acute response seen in the distinct environment was significantly attenuated by 1 hr of habituation to the test environment, and completely abolished by 6--8 hr of habituation. Also, as little as 1 hr of habituation completely prevented the development of a conditioned rotational response. In contrast, neither 1 nor 6--8 hr of habituation had any effect on the ability of amphetamine to induce robust behavioral sensitization. It is concluded that the ability of a distinct environment to facilitate sensitization to amphetamine can be dissociated from its effect on acute drug responsiveness and from the ability of drug-associated environmental stimuli to elicit a conditioned response. Possible mechanisms by which a distinct environment facilitates sensitization are discussed. (+info)Bronchodilator therapy and hyperactivity in preschool children. (3/63)
The common report of parents of asthmatic children that inhaled/nebulised salbutamol causes overactive behaviour was investigated. Nineteen children were assessed in a standardised setting before and after the administration of nebulised salbutamol and placebo. Neither parental report nor observer ratings suggested any significant increase in the child's level of activity. (+info)The bioavailability and pharmacokinetics of subcutaneous, nebulized and oral morphine-6-glucuronide. (4/63)
AIMS: Morphine-6-glucuronide (M6G), one of the active metabolites of morphine, has attracted considerable interest as a potent opioid analgesic with an apparently superior therapeutic index. To date studies have used the intravenous route, which is generally unacceptable in the treatment of cancer related pain. The aim of this study was to define the pharmacokinetics, toxicity and cardio-respiratory effects of three alternative routes of administration of M6G. METHODS: Ten healthy volunteers participated in an open randomized study. Subjects received M6G 2 mg as an intravenous bolus, 20 mg orally, 2 mg subcutaneously and 4 mg by the nebulized route. Pulse, blood pressure, respiratory rate and peak flow rate were monitored and subjective toxicity recorded on rating and visual analogue scales. RESULTS: After i.v. M6G the mean (+/- s.d.) AUC(0,infinity) standardized to a dose of 1 mg was 223 +/- 57 nmol l(-1) h, mean elimination half-life was 1.7 +/- 0.7 h and the mean clearance was 157 +/- 46 ml min(-1). These parameters were virtually identical after subcutaneous administration which had a bioavailability (F(0,infinity)) of 102 +/- 35% (90% CI 82, 117%) and t(max) of 0.5 +/- 0.2 h. The mean bioavailability of nebulized M6G was 6 +/- 2% (90% CI 4, 7%) with a t(max) of 1.2 +/- 0.8 h. Following oral M6G two plasma M6G peaks were seen in 7 of the 10 subjects, the first with a t(max) of 3.1 (+/- 0.9) h. The second peak had a t(max) of 13.4 (+/-5.0) h, started approximately 4 h after dosing, and was associated with the detection of plasma M3G and morphine, suggesting that M6G was significantly hydrolysed in the gut to morphine, which was then glucuronidated following absorption. Although the overall mean bioavailability was 11 +/- 3% (90% CI 9, 12%), confining the analysis to data from the first peak suggested a bioavailability of directly absorbed M6G of only 4 +/- 4%. Apart from a characteristic dysphoria following intravenous and subcutaneous M6G, there was no significant toxicity. CONCLUSIONS: With the minimal toxicity reported in this and previous studies, subcutaneous infusion of M6G may potentially provide clinically useful analgesia for advanced cancer pain. Nebulized M6G is not significantly absorbed via the lungs, and if opiates are shown to have a local effect in the lung, reducing the sensation of breathlessness, then nebulized administration is likely to minimize systemic effects. Oral M6G has poor bioavailability, but is significantly hydrolysed in the gut to morphine, which is subsequently glucuronidated following absorption. This circuitous route accounts for the majority of systemically available M6G after oral administration. (+info)Comparison of caudal and intravenous clonidine in the prevention of agitation after sevoflurane in children. (5/63)
BACKGROUND: In children, sevoflurane anaesthesia is associated with postanaesthetic agitation, which is treated mainly with opioids. We compared the effectiveness of epidural and i.v. clonidine in the prevention of this postanaesthetic agitation. METHODS: Eighty children aged 3-8 yr (ASA I-II) received standardized general anaesthesia with inhaled sevoflurane and caudal epidural block with 0.175% bupivacaine 1 ml kg-1 for minor surgery. The children were assigned randomly to four groups: (I) clonidine 1 microgram kg-1 added to caudal bupivacaine; (II) clonidine 3 micrograms kg-1 added to caudal bupivacaine; (III) clonidine 3 micrograms kg-1 i.v. and caudal bupivacaine; and (IV) caudal block with bupivacaine, no clonidine (control). A blinded observer assessed the behaviour of the children during the first postoperative hour. Secondary end-points were the time to fitness for discharge from the postanaesthesia care unit, and haemodynamic and respiratory variables. RESULTS: The incidence of agitation was 22, 0, 5 and 39% in groups I, II, III and IV respectively (P < 0.05 for groups II and III compared with group IV). During the first hour after surgery, patients in groups II and III had significantly lower scores for agitation than group IV patients. Time to fitness for discharge did not differ between the four groups. CONCLUSIONS: Clonidine 3 micrograms kg-1 prevented agitation after sevoflurane anaesthesia, independently of the route of administration. The effect of clonidine appears to be dose-dependent, as an epidural dose of 1 microgram kg-1 failed to reduce it. (+info)Nithsdale Schizophrenia Surveys 23: movement disorders. 20-year review. (6/63)
BACKGROUND: In the past 10 years the new atypical antipsychotic drugs have stimulated further interest in the pharmacological management of schizophrenia. The risk of movement disorders has been reported to be less with these new agents. AIMS: To examine the current prevalence of movement disorders among all people with schizophrenia in a discrete geographical area, to compare the prevalence in patients receiving and not receiving atypical antipsychotic drugs; and to compare current prevalence with prevalence over the past 20 years. METHOD: In Nithsdale, south-west Scotland, in 1999/2000, we replicated previous studies by using the Abnormal Involuntary Movements Scale, Simpson-Angus scale and Barnes Akathisia Rating Scale to measure tardive dyskinesia, parkinsonism and akathisia, respectively. Mental state was assessed by the Positive and Negative Syndrome Scale. RESULTS: In 136 patients the prevalence of probable tardive dyskinesia was 43%, of parkinsonism 35% and of akathisia 15%. Parkinsonism was present as often in those receiving atypicals as in those receiving standard oral antipsychotics. The prevalence of tardive dyskinesia has doubled over 20 years. CONCLUSIONS: Movement disorders remain significant problems for patients despite the introduction of atypical antipsychotic drugs. (+info)Akathisia--diagnostic dilemma and behavioral treatment. (7/63)
Akathisia, an involuntary movement disorder resulting from exposure to antipsychotics, is characterized by subjective restlessness and a strong desire to move about. The diagnosis is often complicated by the overlapping symptoms of pseudoakathisia, chronic akathisia and tardive dyskinesia. This report deals with a patient with schizophrenia who developed akathisia after exposure to antipsychotics. Later, she developed movements that were more like pseudoakathisia and tardive dyskinesia rather than acute akathisia. On failure of anti-akathisia medication, she was treated with a behavioral regime to which her akathisia responded. This behavioral regime used the technique of distraction as a primary tool. This case report highlights the diagnostic difficulties in akathisia and the application of behavioral treatment for akathisia that is non-responsive to anti-akathisia medication. (+info)The effects of temporary inactivation of the core and the shell subregions of the nucleus accumbens on prepulse inhibition of the acoustic startle reflex and activity in rats. (8/63)
The nucleus accumbens can be dissociated into at least two subregions: a 'core' and a 'shell'. Using temporary chemical inactivation of these subregions, we investigated whether they are differentially involved in the regulation of prepulse inhibition (PPI) of the acoustic startle reflex and activity. For this purpose, rats were bilaterally implanted with guide cannulae aimed at either the core or the shell and infused with the GABA(A) receptor agonist muscimol (0.5 microg/0.2 microl per side). The control group consisted of vehicle infused and unoperated rats. To ascertain the region selectivity of the infusions, 0.2 microl of [3H]muscimol was infused into either the core or the shell of an additional group of rats. The behavioral results demonstrated that in comparison to the control group, inactivation of the core led to a loss of the prepulse intensity dependency of PPI. Moreover, core inactivation resulted in akinesia directly after infusion, but in hyperactivity 24 and 72 h thereafter in contrast to the control group. In both experiments, inactivation of the shell was ineffective compared to controls. Analysis of the autoradiograms revealed that the spread of drug into the other subregion was minimal, supporting the region selectivity of the inactivation. These results lend further support to the existence of a functional dissociation between the core and the shell, with the former being preferentially involved in PPI and locomotion. The persistent hyperactivity after the muscimol infusion into the core could be explained by compensatory mechanisms taking place in the nucleus accumbens. (+info)Drug-induced akathisia is a type of movement disorder that is a side effect of certain medications. The term "akathisia" comes from the Greek words "a-," meaning "without," and "kathisia," meaning "sitting." It is characterized by a subjective feeling of restlessness and an uncontrollable urge to be in constant motion, accompanied by objective motor symptoms such as fidgeting, rocking, or pacing.
Drug-induced akathisia is most commonly associated with the use of antipsychotic medications, particularly those that block dopamine receptors in the brain. Other drugs that have been linked to akathisia include certain antidepressants, anti-nausea medications, and some beta blockers used to treat heart conditions.
The symptoms of drug-induced akathisia can range from mild to severe and may include:
* A subjective feeling of inner restlessness or anxiety
* An uncontrollable urge to move, such as fidgeting, rocking, or pacing
* Difficulty sitting still or lying down
* Agitation and irritability
* Sleep disturbances
* Depression or dysphoria
* Suicidal thoughts or behaviors (in severe cases)
The symptoms of drug-induced akathisia can be distressing and may contribute to noncompliance with medication treatment. In some cases, the symptoms may resolve on their own after a period of time, but in other cases, they may persist or worsen, requiring a change in medication or the addition of other medications to manage the symptoms. It is important for individuals who are taking medications that have been associated with akathisia to report any new or worsening symptoms to their healthcare provider as soon as possible.
Psychomotor agitation is a state of increased physical activity and purposeless or semi-purposeful voluntary movements, usually associated with restlessness, irritability, and cognitive impairment. It can be a manifestation of various medical and neurological conditions such as delirium, dementia, bipolar disorder, schizophrenia, and substance withdrawal. Psychomotor agitation may also increase the risk of aggressive behavior and physical harm to oneself or others. Appropriate evaluation and management are necessary to address the underlying cause and alleviate symptoms.
Drug-induced dyskinesia is a movement disorder that is characterized by involuntary muscle movements or abnormal posturing of the body. It is a side effect that can occur from the long-term use or high doses of certain medications, particularly those used to treat Parkinson's disease and psychosis.
The symptoms of drug-induced dyskinesia can vary in severity and may include rapid, involuntary movements of the limbs, face, or tongue; twisting or writhing movements; and abnormal posturing of the arms, legs, or trunk. These symptoms can be distressing and negatively impact a person's quality of life.
The exact mechanism by which certain medications cause dyskinesia is not fully understood, but it is thought to involve changes in the levels of dopamine, a neurotransmitter that plays a key role in regulating movement. In some cases, adjusting the dose or switching to a different medication may help alleviate the symptoms of drug-induced dyskinesia. However, in severe cases, additional treatments such as deep brain stimulation or botulinum toxin injections may be necessary.
Antipsychotic agents are a class of medications used to manage and treat psychosis, which includes symptoms such as delusions, hallucinations, paranoia, disordered thought processes, and agitated behavior. These drugs work by blocking the action of dopamine, a neurotransmitter in the brain that is believed to play a role in the development of psychotic symptoms. Antipsychotics can be broadly divided into two categories: first-generation antipsychotics (also known as typical antipsychotics) and second-generation antipsychotics (also known as atypical antipsychotics).
First-generation antipsychotics, such as chlorpromazine, haloperidol, and fluphenazine, were developed in the 1950s and have been widely used for several decades. They are generally effective in reducing positive symptoms of psychosis (such as hallucinations and delusions) but can cause significant side effects, including extrapyramidal symptoms (EPS), such as rigidity, tremors, and involuntary movements, as well as weight gain, sedation, and orthostatic hypotension.
Second-generation antipsychotics, such as clozapine, risperidone, olanzapine, quetiapine, and aripiprazole, were developed more recently and are considered to have a more favorable side effect profile than first-generation antipsychotics. They are generally effective in reducing both positive and negative symptoms of psychosis (such as apathy, anhedonia, and social withdrawal) and cause fewer EPS. However, they can still cause significant weight gain, metabolic disturbances, and sedation.
Antipsychotic agents are used to treat various psychiatric disorders, including schizophrenia, bipolar disorder, major depressive disorder with psychotic features, delusional disorder, and other conditions that involve psychosis or agitation. They can be administered orally, intramuscularly, or via long-acting injectable formulations. The choice of antipsychotic agent depends on the individual patient's needs, preferences, and response to treatment, as well as the potential for side effects. Regular monitoring of patients taking antipsychotics is essential to ensure their safety and effectiveness.
Metoclopramide is a medication that is primarily used to manage gastrointestinal disorders. It is classified as a dopamine antagonist and a prokinetic agent, which means it works by blocking the action of dopamine, a chemical in the brain that can slow down stomach and intestine function.
The medical definition of Metoclopramide is:
A synthetic congener of procainamide, used as an antiemetic and to increase gastrointestinal motility. It has a antidopaminergic action, binding to D2 receptors in the chemoreceptor trigger zone and stomach, and it may also block 5HT3 receptors at intrapyloric and central levels. Its actions on the gut smooth muscle are mediated via cholinergic muscarinic receptors. (Source: Dorland's Medical Dictionary)
Metoclopramide is commonly used to treat conditions such as gastroesophageal reflux disease (GERD), gastritis, and gastroparesis, which is a condition that affects the normal movement of food through the digestive tract. It can also be used to prevent nausea and vomiting caused by chemotherapy or radiation therapy.
Like any medication, Metoclopramide can have side effects, including drowsiness, restlessness, and muscle spasms. In some cases, it may cause more serious side effects such as tardive dyskinesia, a condition characterized by involuntary movements of the face, tongue, or limbs. It is important to use Metoclopramide only under the supervision of a healthcare provider and to follow their instructions carefully.
Basal ganglia diseases are a group of neurological disorders that affect the function of the basal ganglia, which are clusters of nerve cells located deep within the brain. The basal ganglia play a crucial role in controlling movement and coordination. When they are damaged or degenerate, it can result in various motor symptoms such as tremors, rigidity, bradykinesia (slowness of movement), and difficulty with balance and walking.
Some examples of basal ganglia diseases include:
1. Parkinson's disease - a progressive disorder that affects movement due to the death of dopamine-producing cells in the basal ganglia.
2. Huntington's disease - an inherited neurodegenerative disorder that causes uncontrolled movements, emotional problems, and cognitive decline.
3. Dystonia - a movement disorder characterized by sustained or intermittent muscle contractions that cause twisting and repetitive movements or abnormal postures.
4. Wilson's disease - a rare genetic disorder that causes excessive copper accumulation in the liver and brain, leading to neurological and psychiatric symptoms.
5. Progressive supranuclear palsy (PSP) - a rare brain disorder that affects movement, gait, and balance, as well as speech and swallowing.
6. Corticobasal degeneration (CBD) - a rare neurological disorder characterized by progressive loss of nerve cells in the cerebral cortex and basal ganglia, leading to stiffness, rigidity, and difficulty with movement and coordination.
Treatment for basal ganglia diseases varies depending on the specific diagnosis and symptoms but may include medication, surgery, physical therapy, or a combination of these approaches.
Secondary Parkinson's disease, also known as acquired or symptomatic Parkinsonism, is a clinical syndrome characterized by the signs and symptoms of classic Parkinson's disease (tremor at rest, rigidity, bradykinesia, and postural instability) but caused by a known secondary cause. These causes can include various conditions such as brain injuries, infections, drugs or toxins, metabolic disorders, and vascular damage. The underlying pathology of secondary Parkinson's disease is different from that of classic Parkinson's disease, which is primarily due to the degeneration of dopamine-producing neurons in a specific area of the brain called the substantia nigra pars compacta.
Diphenhydramine is an antihistamine medication used to relieve symptoms of allergies, such as sneezing, runny nose, and itchy or watery eyes. It works by blocking the action of histamine, a substance in the body that causes allergic reactions. Diphenhydramine can also be used to treat motion sickness, insomnia, and symptoms of the common cold.
In addition to its antihistamine effects, diphenhydramine also has anticholinergic properties, which means it can help to reduce secretions in the nose and throat, and may have a drying effect on the mouth and eyes. It is available over-the-counter in various forms, including tablets, capsules, liquid, and topical creams or ointments.
It's important to note that diphenhydramine can cause drowsiness, so it should be used with caution when operating heavy machinery or driving a vehicle. It may also interact with other medications, so it's important to speak with a healthcare provider before taking this medication.
Affective disorders, psychotic are a category of mental health conditions characterized by significant disturbances in mood, thinking, and behavior. These disorders combine the symptoms of both mood disorders (such as depression or bipolar disorder) and psychotic disorders (such as schizophrenia).
In psychotic affective disorders, individuals experience severe changes in their mood, such as prolonged periods of depression or mania, along with psychotic features like hallucinations, delusions, or disorganized thinking and speech. These symptoms can significantly impair a person's ability to function in daily life and may require intensive treatment, including medication and therapy.
Examples of psychotic affective disorders include:
1. Psychotic Depression: A severe form of major depressive disorder that includes psychotic symptoms like delusions or hallucinations, often with a theme of guilt or worthlessness.
2. Bipolar Disorder with Psychotic Features: During manic or depressive episodes, some individuals with bipolar disorder may experience psychotic symptoms such as delusions or hallucinations. These symptoms can vary in intensity and may require hospitalization and intensive treatment.
3. Schizoaffective Disorder: A mental health condition that includes features of both schizophrenia and a mood disorder, such as depression or bipolar disorder. Individuals with this disorder experience psychotic symptoms like hallucinations and delusions, along with significant changes in mood.
It is essential to seek professional help if you suspect you or someone you know may have a psychotic affective disorder. Early intervention and treatment can significantly improve outcomes and quality of life.
Dibenzothiazepines are a class of heterocyclic chemical compounds that contain a dibenzothiazepine ring structure. This structure is composed of a benzene ring fused to a thiazepine ring, which is itself formed by the fusion of a benzene ring and a diazepine ring (a seven-membered ring containing two nitrogen atoms).
In the medical field, dibenzothiazepines are known for their pharmacological properties and have been used in the development of various drugs. Some dibenzothiazepine derivatives exhibit antipsychotic, anxiolytic, and anticonvulsant activities. However, due to their potential for adverse effects and the availability of safer alternatives, they are not widely used in clinical practice today.
It is important to note that specific dibenzothiazepine compounds may have unique properties and uses beyond their general classification as a chemical class. Always consult medical literature or healthcare professionals for accurate information on specific drugs or compounds.
Benzodiazepines are a class of psychoactive drugs that have been widely used for their sedative, hypnotic, anxiolytic, anticonvulsant, and muscle relaxant properties. They act by enhancing the inhibitory effects of gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the central nervous system.
Benzodiazepines are commonly prescribed for the treatment of anxiety disorders, insomnia, seizures, and muscle spasms. They can also be used as premedication before medical procedures to produce sedation, amnesia, and anxiolysis. Some examples of benzodiazepines include diazepam (Valium), alprazolam (Xanax), clonazepam (Klonopin), lorazepam (Ativan), and temazepam (Restoril).
While benzodiazepines are effective in treating various medical conditions, they can also cause physical dependence and withdrawal symptoms. Long-term use of benzodiazepines can lead to tolerance, meaning that higher doses are needed to achieve the same effect. Abrupt discontinuation of benzodiazepines can result in severe withdrawal symptoms, including seizures, hallucinations, and anxiety. Therefore, it is important to taper off benzodiazepines gradually under medical supervision.
Benzodiazepines are classified as Schedule IV controlled substances in the United States due to their potential for abuse and dependence. It is essential to use them only as directed by a healthcare provider and to be aware of their potential risks and benefits.
Movement disorders are a group of neurological conditions that affect the control and coordination of voluntary movements. These disorders can result from damage to or dysfunction of the cerebellum, basal ganglia, or other parts of the brain that regulate movement. Symptoms may include tremors, rigidity, bradykinesia (slowness of movement), akathisia (restlessness and inability to remain still), dystonia (sustained muscle contractions leading to abnormal postures), chorea (rapid, unpredictable movements), tics, and gait disturbances. Examples of movement disorders include Parkinson's disease, Huntington's disease, Tourette syndrome, and dystonic disorders.
Cholinergic antagonists, also known as anticholinergics or parasympatholytics, are a class of drugs that block the action of the neurotransmitter acetylcholine in the nervous system. They achieve this by binding to and blocking the activation of muscarinic acetylcholine receptors, which are found in various organs throughout the body, including the eyes, lungs, heart, gastrointestinal tract, and urinary bladder.
The blockade of these receptors results in a range of effects depending on the specific organ system involved. For example, cholinergic antagonists can cause mydriasis (dilation of the pupils), cycloplegia (paralysis of the ciliary muscle of the eye), tachycardia (rapid heart rate), reduced gastrointestinal motility and secretion, urinary retention, and respiratory tract smooth muscle relaxation.
Cholinergic antagonists are used in a variety of clinical settings, including the treatment of conditions such as Parkinson's disease, chronic obstructive pulmonary disease (COPD), asthma, gastrointestinal disorders, and urinary incontinence. Some common examples of cholinergic antagonists include atropine, scopolamine, ipratropium, and oxybutynin.
It's important to note that cholinergic antagonists can have significant side effects, particularly when used in high doses or in combination with other medications that affect the nervous system. These side effects can include confusion, memory impairment, hallucinations, delirium, and blurred vision. Therefore, it's essential to use these drugs under the close supervision of a healthcare provider and to follow their instructions carefully.
Schizophrenia is a severe mental disorder characterized by disturbances in thought, perception, emotion, and behavior. It often includes hallucinations (usually hearing voices), delusions, paranoia, and disorganized speech and behavior. The onset of symptoms typically occurs in late adolescence or early adulthood. Schizophrenia is a complex, chronic condition that requires ongoing treatment and management. It significantly impairs social and occupational functioning, and it's often associated with reduced life expectancy due to comorbid medical conditions. The exact causes of schizophrenia are not fully understood, but research suggests that genetic, environmental, and neurodevelopmental factors play a role in its development.
Diagnostic errors refer to inaccurate or delayed diagnoses of a patient's medical condition, which can lead to improper or unnecessary treatment and potentially serious harm to the patient. These errors can occur due to various factors such as lack of clinical knowledge, failure to consider all possible diagnoses, inadequate communication between healthcare providers and patients, and problems with testing or interpretation of test results. Diagnostic errors are a significant cause of preventable harm in medical care and have been identified as a priority area for quality improvement efforts.
A neurological examination is a series of tests used to evaluate the functioning of the nervous system, including both the central nervous system (the brain and spinal cord) and peripheral nervous system (the nerves that extend from the brain and spinal cord to the rest of the body). It is typically performed by a healthcare professional such as a neurologist or a primary care physician with specialized training in neurology.
During a neurological examination, the healthcare provider will assess various aspects of neurological function, including:
1. Mental status: This involves evaluating a person's level of consciousness, orientation, memory, and cognitive abilities.
2. Cranial nerves: There are 12 cranial nerves that control functions such as vision, hearing, smell, taste, and movement of the face and neck. The healthcare provider will test each of these nerves to ensure they are functioning properly.
3. Motor function: This involves assessing muscle strength, tone, coordination, and reflexes. The healthcare provider may ask the person to perform certain movements or tasks to evaluate these functions.
4. Sensory function: The healthcare provider will test a person's ability to feel different types of sensations, such as touch, pain, temperature, vibration, and proprioception (the sense of where your body is in space).
5. Coordination and balance: The healthcare provider may assess a person's ability to perform coordinated movements, such as touching their finger to their nose or walking heel-to-toe.
6. Reflexes: The healthcare provider will test various reflexes throughout the body using a reflex hammer.
The results of a neurological examination can help healthcare providers diagnose and monitor conditions that affect the nervous system, such as stroke, multiple sclerosis, Parkinson's disease, or peripheral neuropathy.
Trihexyphenidyl
