• Simple: They include only one muscle group

• Eyeblink
• Shoulder shrug
• Head jerk

• Complex: They make use of more than one muscle group, and the body of the face of the affected individual may contort.

• Touching someone
• Jump
• Sniff
• Making an indecent gesture

When does it usually occur and how common is it?

The initial symptoms of Tourette’s generally surface first in one’s childhood, with the average onset is found to be between three and nine years of age. All ethnic groups suffer from this disease and men suffer as much as thrice or four times in comparison with women. It is observed that two hundred thousand Americans suffer from the most severe type of this disorder and one in every hundred persons display less complex and comparatively mild symptoms like vocal or chronic motor tics. In spite of the fact that it is a chronic condition whose symptoms tend to last a lifetime, a vast majority of the patients experience the worst during their early teen years, with improvement happening in their late teen years and succeeding into adulthood.

Causes of Tourette Syndrome

While the researchers are yet to discover what causes Tourette’s, present studies suggest any abnormality in any one or more of the following parts of the human body may be responsible for its manifestation.

• Certain regions in the brain

• Basal ganglia
• Cortex
• Frontal lobes

• The circuits interconnecting the areas mentioned above
• The neurotransmitters that regulate the communication among the nerve cells

• Dopamine
• Norepinephrine
• Serotonin

Symptoms of Tourette Syndrome

It is vital to understand that the primary symptom of Tourette’s is tics, and some of them are so diminutive that they are barely noticeable, while others are evident and occur often; and excitement, sickness, or stress do tend to make them worse. Tics that are more severe can affect one’s work or social life and can be embarrassing. The tics can be classified into the following two types.

Motor Tics that Include Movement

• Head or arm jerking
• Making a face
• Blinking
• Shoulder shrugging
• Mouth twitching

Vocal tics

• Clearing one’s throat
• Yelping or barking
• Grunting
• Coughing
• Shouting
• Repeating anything that is uttered by others
• Swearing
• Sniffing

Diagnosis

No specific tests exist for the diagnosis and it is done after evaluating the history of one’s symptoms and signs. The following factors are taken into account at the time of performing a clinical diagnosis.

• Both the vocal and motor tics are present, but not necessarily at the same point of time
• The tics are occurring several times daily, almost intermittently or every day, and last over a year
• The tics start before the age of eighteen
• No medications, other chemical substances, or any medical conditions are causing the tics to happen
• Tics aren’t caused by medications, other substances or another medical condition

The specialist may ignore the diagnosis of Tourette’s, as the signs can resemble symptoms of other conditions. Sniffling might be associated with allergies in the beginning, or eye blinking could be attributed to vision problems.

Both the vocal and motor tics can be induced by other medical conditions excluding the Tourette syndrome. The health care professional might also recommend the following test to eliminate other probable causes.

• MRI
• Blood tests

Differential Diagnosis

• Dystonias

• Choreas
• Sydenham’s Chorea
• Idiopathic Dystonia
• Huntington’s
• Neuroacanthocytosis
• Duchenne Muscular Dystrophy (DMD)
• Hallervorden-Spatz syndrome (HSS)
• Wilson’s
• Tuberous sclerosis
• Down syndrome
• XYY syndrome
• Fragile X syndrome
• Klinefelter syndrome
• Lesch-Nyhan syndrome (LNS)
• Substance induction
• Stroke
• Trauma
• Encephalitis
• Carbon Monoxide (CO) poisoning
• Developmental disorders
• Autism spectrum disorders (ASDs)
• Stereotypic movement disorders (SMDs)

Treatments

The tics can be found to be mild in many cases, and hence, they do not require any treatment. But if they start posing problems; a medical practitioner may suggest medication, and it can take some time to gauge the right dose, the one that will effectively manage the tics albeit any adverse effects.

The following medications are often prescribed.

Brand name: Generic name

• Haldol: Haloperidol
• Orap: Pimozide
• Prolixin: Fluphenazine

Note: These drugs work on dopamine for regulating the tics.

• Prozac: Fluoxetine
• Zoloft: Sertraline
• Paxil: Paroxetine

Note: These drugs reduce obsessive-compulsive symptoms, sadness, and anxiety.

• Tenex or Intuniv: Guanfacine
• Catapres: Clonidine

Note: High blood pressure medicines like these are also used to treat the tics.

One may also consider talk therapy along with the prescribed medication. A counselor or a psychologist can guide the patient and impart training on managing the social issues that the tics and other associated symptoms may cause. The affected individuals can also get benefitted from behavior therapy. A specific kind, known as the habit-reversal training or habit reprogramming teaches people with Tourette’s how to identify an incoming tic and then proceed in such a manner that stops it.

Prevention of Tourette Syndrome

Though it is not possible to prevent Tourette syndrome, early detection and prompt treatment can help to mitigate the severity of the disease and prevent a number of issues caused by this disorder.

Prognosis

The condition in a large number of people improves in their late teens or early twenties. As a consequence, some of them may no longer require tic-suppressive medication or literally become symptom-free. Although Tourette’s is usually a chronic illness that lasts a lifetime, it is not degenerative. The life expectancy of individuals who are diagnosed with Tourette syndrome is found to be statistically normal.

Also, this disease does not have any role in impairing one’s intelligence. It is worthwhile to note that a person affected with this syndrome can still face issues from other neurobehavioral disorders like ADHD, depression, OCD, panic attacks, generalized anxiety, and mood swings; irrespective of the fact that the symptoms associated with Tourette’s typically decrease with age.

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Other Names of Strømme Syndrome

• Apple peel syndrome
• Apple peel anomalies
• CILD31
• Ciliary dyskinesia
• Jejunal atresia

Ocular anomalies (including varying degrees of)

• Angular dysgenesis
• Corneal leukemia
• Hypoplasia
• Micro cornea
• Cataracts
• Anterior synechiae
• Sclera cornea
• Iris colobomas

The clinical characteristics of this disease are illustrated below in short.

Ocular features

In Strømme syndrome, the core complex incorporates intestinal atresia as well as ocular abnormalities related to the anterior segment. The ocular anomalies involve varying degrees of angle dysgenesis, corneal leukoma, anterior synechiae, iris hypoplasia and colobomas, sclera cornea, cataracts, and micro cornea. Also, microphthalmia, optic nerve hypoplasia, and tortuous retinal vessels may be present. Deep-set eyes and hypertelorism have been reported. No cases of glaucoma have been described. Most of the patients have been pretty young for RAT or reliable acuity testing.

Systemic features

The phenotype is pretty variable. It is observed that the ears are low-set and large most of the time. Microcephaly is present most of the time accompanied by micrognathia and a cleft palate. The intestinal atresia appears involving the jejunum mainly and is typically surgically correctable. Intestinal malrotation has also been noted, and the duodenum may too be involved. Myopathic changes are found in the myocardium along with a small amount of cardiomyocytes. Microcephaly is apparently seen to be progressive. Renal hydronephrosis and hypodysplasia have been stated. Short stature has also been described, and when it comes to the development of affected individuals, the amount of delay is found to be highly variable.

Causes of Strømme Syndrome

Strømme syndrome is a rare hereditary disease caused by a mutation in the Centromere protein F at chromosome 1q41 (CENPF 1q41) gene. This mutation happens in both the persons involved in sexual congress, and as a consequence, it is transferred to the offspring/s. To put things into perspective, one out of four babies will inherit this syndrome, provided each parent has one single mutation. Mutation in this ARD means a complete alteration of the particular gene, and it is the one and only cause of Strømme syndrome.

Symptoms

• Low set ears
• Hypertelorism
• Ear malformation
• Congenital eye anomaly
• Hypoplastic mandible condyle
• Microcephaly
• Abnormality in the skeleton system
• Abnormality in the respiratory system
• Abnormality of the nervous system
• Abnormality of the digestive system
• Ciliary dyskinesia
• Hydrocephalus
• Cerebellar hypoplasia
• Corpus callosum agenesis
• Duodenal atresia
• Short columella
• Hypoplasic mandible condyle
• Cleft palate
• Smaller head than usual
• Longer neck than usual

Diagnosis

The syndrome was first stated by Norwegian pediatrician Peter Strømme et al. in 1993 in biological siblings presenting with microcephaly, apple peel intestinal atresia, and ocular anomalies. The etiology is unknown to date. Strømme syndrome is an ARD caused by a mutated CENPF leading to a wide gamut of phenotypic spectrum. Family-based WES or whole-exome sequencing is employed case-to-case basis to identify the truncating genetic mutations in CENPF, i.e., the centrosome gene.

Differential diagnosis

As there are only a dozen cases of Strømme syndrome in the entire world, the question of performing a differential diagnosis does not arise here.

Treatments

Strømme syndrome cannot be treated because it is an RCD or recessive congenital disorder that happens due to mutated genes. Nonetheless; the associated conditions; such as intestinal abnormalities, head abnormalities, and visual impairment can be managed with medication. Intestinal surgery is sometimes done if the patient is a child.

Medications

Medications that are used for treating this disease include hormone therapy with letrozole, estrogens, dopamine, memantine, etc. Hormonal antagonists are too used. Other agents include the application of analgesics, protein kinase inhibitors, steroid synthesis inhibitors, anti-microbial drugs and anti-viral medicines.

The unique case study of Ruby Ardolf is presented below in brief.

Ruby Ardolf is a lively twelve-year-old girl from Lakeville in Minnesota, who is born with Strømme syndrome.

Ruby’s beginnings were pretty rough, who happened to be an unplanned pregnancy. Her father did not second his spouse Angie’s decision not to terminate the pregnancy medically. Also, Angie’s first ultrasound did trouble the technician, and every new ultrasound translated to the more bad news. Among a multitude of predictions and diagnoses made by the doctors, they announced that the baby might never talk or walk.

However; much to her luck, Ruby had had a devoted fan, and she was none other than the girl’s mother. When presented with the alternative of medical termination of her pregnancy, Angie promptly declined.

Ruby is now thirteen years old and attends formal schooling just like any other regular student does. Throughout the previous twelve years, the specialists kept making several predictions about her future, and this sixth-grader proved those people all wrong. The girl started to walk at the tender age of three and began to talk when she was merely four years old.

Prevention

As Strømme syndrome is an ARD or autosomal recessive disorder, where the responsible gene mutates in both the members of the genetic pair, this disease cannot be prevented.

Prognosis

Infants typically do well after intestinal surgery. The outcomes of corneal transplants are not reported to date. The prognosis for this rare genetic disease is highly variable. Some people develop and continue to function near average, while the ones with more severity may not be alive after infancy or beyond the early childhood years.

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The episodes of rapid heartbeats generally are not regarded as life-threatening. Nonetheless, serious heart issues can develop. Timely treatment can prevent or stop such incidences. A catheter-guided ablation procedure can permanently fix the problems related to one’s heart rhythm.

A vast majority of people having an additional electrical pathway do not experience fast heartbeat at all. This condition, known as the Wolff-Parkinson-White or WPW pattern, is discovered by chance only at the time of a heart examination. While the WPW pattern is deemed harmless most of the time, healthcare professionals might suggest further evaluation in kids with WPW pattern, before they are allowed to take part in physically demanding sports.

Causes of Wolff Parkinson White Syndrome

The human heart is made of one pair of upper and lower chambers, each, which are known as the left and right atrium and the left and right ventricle respectively. The sophisticated bioelectrical circuitry of the heart signals it when to contract and if an additional electrical connection is present inside this vital organ, the entire circuit is shorted, causing the heart to beat irregularly or even too fast.

In any WPWS patient, the atria and the ventricle cannot communicate properly, and the electrical impulses traverse the normal electrical node of that person’s heart, making the ventricle to contract earlier than it should. WPWS affects one to three in every thousand people.

It is still an unsolved medical mystery what makes this additional electrical pathway to form. However, it is observed that a small number of persons suffering from WPWS carry mutated genes, and others are found to be born with heart defects. In WPWS infants, about two in every ten are diagnosed with Ebstein’s anomaly, which can be attributed to the abnormalities of the tricuspid valve located on the right part of the heart.

Symptoms

People corresponding to all age groups, including the infants, can experience WPWS symptoms. Symptoms of WPWS are the outcome of a quickly beating heart, and they usually make a maiden appearance in individuals in their twenties or teens.

Non-severe symptoms

• Experiencing pounding, fluttering, or rapid heartbeats
• Breathing issues (shortness)
• Lightheadedness or dizziness
• Fatigue
• Fainting
• Anxiety

An incidence of a very rapidly beating heart can begin all of a sudden and could last for as little as few seconds or as much as several hours. Such episodes can happen while at rest or at the time of exercise, and alcohol and any other stimulants including caffeine may act as a trigger for a number of people.

Over time, WPWS symptoms may cease to exist in up to one-fourth of people who had had the syndrome.

More critical symptoms

About one to three in every ten individuals diagnosed with WPWS occasionally experience a kind of irregular heartbeat, i.e., atrial fibrillation; and the following symptoms and signs may occur in such a group of people.

• Chest tightness
• Chest pain
• Fainting
• Difficulty breathing

Symptoms (infants)

• Ashen color
• Rapid breathing
• Irritability or restlessness
• Poor eating

Diagnosis

• Electrocardiogram or ECG: Tiny sensors attached on the patient’s arms and chest record the electrical signals that travels through that person’s heart. The medical practitioner looks for patterns that suggest that an additional electrical pathway is present in the heart of the person subjected to an ECG.
• Portable ECG or pECG: The whole procedure is arranged at home, and the Holter monitor registers the activities of the patient’s heart for twenty-four hours. When the subject is experiencing a rapid increase in heart rate, an event monitor records that activity.
• Electrophysiological testing or EPT: Catheters armed with electrodes are made to pass through the blood vessels up to several areas in the patient’s heart. The electrodes can specifically map how the electrical impulses are spreading at the time of every heartbeat, and also identify the existence of any additional electrical pathway.

Differential Diagnosis

Diagnosis of hypertrophy, myocardial infarction or MI, and bundle branch block or BBB in instances of WPW syndrome are all obscured.

• Type A WPWS should be distinguishable from the following heart-related conditions
• Right ventricular hypertrophy or RVH
• Right BBB or RBBB
• Inferior MI
• True posterior MI
• Type B WPWS should be distinguishable from the following heart-related conditions
• Left BBB or LBBB
• Inferior MI
• Anterior MI
• WPW syndrome and atrial flutter
• Paroxysmal VT (ventricular tachycardia) or flutter

Treatments

The treatment is decided by various factors, including the frequency and the severity of the symptoms. If the patient does have the WPW pathway, but not any symptoms, then that person is unlikely to receive any surgical procedures or scheduled medication. In case treatment is required, the objective is to slow down a fast heart as soon as it happens and to prevent any such episodes in future.

The specialist may suggest from the following option for treating WPWS.

• Vagal maneuvers: These simple movements of the human body; such as bearing down in the way one has a bowel movement, coughing, and applying a pack of ice on the face; they all affect vagus nerve that helps to regulate the heartbeat.

• Medications: If the vagal movements do not prove to be beneficial in one’s case, then the doctor may consider injecting the patient with an anti-arrhythmic drug.

• Cardioversion: When the first two alternatives prove to be ineffective; the physician may use patches or paddles on the patient’s chest to send a train of electrical impulses to shock the heart, which in turn, helps to restore the normal rhythm.

• Radiofrequency catheter ablation or RCA: It is considered the last line of treatment for WPWS, where catheters are passed through the blood vessels of the patient’s heart. The electrodes fitted at the tip of a thin, flexible tube are heated to melt and dissolve the additional electrical pathway in question permanently.

Prevention

Though it is not possible to prevent the occurrence of WPWS, a large number of people are typically found to be receptive to appropriate therapies, as prescribed by the consultant electrophysiologist or the consultant cardiologist.

Prognosis

The prognosis for this syndrome is excellent. In general, many individuals diagnosed with WPWS may never require any treatment.

When to visit a doctor?

Many medical conditions can trigger arrhythmia, i.e., irregular heartbeat. It is crucial to seek a prompt and accurate diagnosis and appropriate care. Call the doctor immediately if one or some of the following symptoms last beyond a few minutes.

• Irregular or rapid heartbeat
• Chest pain
• Difficulty breathing

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CES impacts a nerve root bundle known as cauda equine, which means horse’s tail in Latin. These nerves are situated at the lumbosacral region, i.e., the bottom end of the spinal cord. They receive and transmit signals to and from one’s feet, legs, and pelvic organs.

Symptoms of this syndrome can manifest all on a sudden or may require weeks or even months to develop. The onset of CES is often illustrated using the characteristic distinctions mentioned below:

• Acute onset: Symptoms rapidly develop within twenty-four hours.
• Gradual onset: Symptoms develop progressively, and they may come and disappear over several weeks or even months.

Causes of Cauda Equina Syndrome

• Primary: CES typically stems from a huge herniated disc that is formed in the lumbar area of the affected Individual. A single excessive injury or strain may lead to a herniated disc. Nonetheless, it is pretty standard for the disc material to degenerate naturally as one age and the supportive ligaments start to weaken. Now, as this process of degeneration progresses, a considerably minor twisting movement or strain can cause a ruptured disk.

Other Likely Causes

• Spinal infections or inflammation (SII)
• Spinal lesions and tumors (SLT)
• Violent injuries on the lower back; such as; auto accidents, falls, gunshots
• Lumbar spinal stenosis (LSS)
• Birth abnormalities
• Spinal anesthesia
• Spinal hemorrhages; for instance; subdural, subarachnoid, epidural
• Spinal arteriovenous malformations (S-AVMs)
• Postoperative lumbar spine surgery complications (PO-LSSC)

Symptoms of Cauda Equina Syndrome

Low back pain

• Local pain: An intense, aching pain caused by an irritation in the vertebral body and soft tissue.
• Leg/radicular pain: A deep, stabbing pain triggered by compressed nerve roots; spreading in the specific areas that are controlled by such compromised nerves, and it is called a dermatomal distribution.
• Sciatica: AN unilateral (in one leg) or bilateral (both the legs) pain originating in the buttocks area and continues to the back of one’s legs and thighs.
• Perineal/saddle paresthesia: Loss of sensation in one’s groin or region of contact when someone is sitting or resting vertically on a saddle.
• Bowel disturbances
• Constipation
• Incontinence: Inability to experience or stop a bowel movement
• The absence of anal tone as well as sensation
• Bladder disturbances
• Urinary hesitancy: Difficulty initiating urination
• Urinary retention: Inability to urinate
• Incontinence: Inability to cease or manage urination
• Decreased urethral sensation: Decreased sensation during urination
• Absent or reduced lower extremity reflexes (LER)
• Weakness in the lower extremity muscle (LEM) and numbness
• Any sudden sexual dysfunction

Diagnosis

• Medical history: Information about the symptoms, health, and activity of the patient is obtained and scrutinized.
• Physical examination: The strength, sensation, reflexes, stability, motion, and alignment of the affected person is assessed.
• Magnetic resonance imaging (MRI)
• Computerized tomography (CT) scan
• X-ray
• Blood tests
• Myelogram: A contrast chemical is injected into the spinal cord, and its x-ray is taken to pinpoint pressure on one’s spinal cord or nerves.

Differential Diagnosis

• Amyotrophic lateral sclerosis or ALS in physical medicine and rehabilitation (ALS-PMR)
• Acute inflammatory demyelinating polyradiculoneuropathy (AIDP)
• Guillain-Barré syndrome (GBS)
• Diabetic neuropathy
• Neoplasms of the spinal cord (NSC)
• Multiple sclerosis
• Neuromuscular and myopathic complications of HIV (NMC-HIV)
• Spinal cord infections (SCI)
• Neurosarcoidosis
• Traumatic peripheral nerve lesions (TPNL)

Treatments

For a patient suffering from acute CES, surgical intervention is likely an immediate requirement. The objective is to relieve the pressure from the spinal nerves for restoring muscle function and sensation to the bladder, legs, and bowel. One of the surgical procedures mentioned below may be performed, depending upon the cause.

Discectomy

It is done to remove a part of the herniated disk, the portion which is putting pressure on the nerves. A small cut is made in the middle area on the back of the patient. The spinal muscles are relocated to expose the bony vertebra further. Then a window of the bone is cut to reveal the nerve root as well as the disc. The part impacting the spinal nerves of the affected individual is carefully removed from the ruptured disk.

Spinal Decompression

Spinal decompression is performed for cases of stenosis, where the ligaments and the bone spurs compressing the nerves are removed. A small hole is drilled in the back of the patient. The bone forming the ceiling of one’s spinal canal is removed. Then bones spurs and soft tissue are removed for creating more room to accommodate the nerves. Tumors, as well as other lesions, can be removed too.

Prevention

Prevention is concentrated on early diagnosis of the symptoms. People should be made aware of the warning signs that could potentially suggest a clinical manifestation of CES, including a change in bladder or bowel functions absence of sensation in one’s groin. However, the cases that are caused by schedule IV drug-induced infections can be prevented, and people should be cautious about not indulging in the usage of illegal schedule IV substances.

Prognosis

Using the ASIA impairment scale

Prognosis can be estimated with the help of the American Spinal Injury Association impairment scale.

• ASIA A: Ninety in every hundred patients are deemed unsuitable to undergo functional ambulation, reciprocal gait is two hundred feet or even more.
• ASIA B: Seventy-two in every hundred patients cannot achieve functional ambulation.
• ASIA C/D: Thirteen in every hundred patients fail to accomplish functional ambulation a year after the occurrence of the injury.

Using the AMI

The ambulatory motor index is also used for predicting the ambulatory capability, and an affected individual with a score of eighteen out of thirty or above has an improved likelihood for community ambulation, where the support will be restricted to a single knee-ankle-foot-orthosis (KAFO).

• A patient having a score of 23.7/30 or more may not require an orthosis.
• A patient having a score of 12/30 or less may need two KAFOs during community ambulation.

Cauda Equina Syndrome Images

References

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Other Names for Neuroleptic Malignant Syndrome

• Drug-Induced Movement Disorder (DMD)
• Hyperthermia
• Neuroleptic-Induced Acute Dystonia (NAD)

Causes

Researchers are yet to discover the inherent cause of NMS. Present theories are limited in their scope to satisfactorily explain all possible clinical manifestations as well as in supporting statistics. An animal model for this syndrome has been conceived, though the construct does not entirely correspond with the one found in humans.

Considering the class of the agents that are involved in cases of NMS, blockade of dopamine receptor is pivotal to a vast majority of the pathogenesis theories. Blockade in the central dopamine receptor (CDR) in the hypothalamus could cause hypothermia as well as other symptoms of dysautonomia. Interference in the nigrostriatal dopamine pathway (NDP) could result in Parkinsonian, type symptoms like tremor and rigidity. Other neurotransmitter systems (NTS), such as epinephrine, acetylcholine, serotonin, and gamma-aminobutyric acid (GABA), are too involved, either actively or implicitly.

Another theory suggests that muscle damage and rigidity indicate a key impact on one’s peripheral muscle system (PMS), which can perhaps be attributed to direct changes taking place in muscle mitochondrial function (MMF). The alteration in itself could likely point towards a defect in the primary skeletal muscle (PSM) or an explicit toxic effect caused on skeletal muscle by neuroleptic medications.

It is also proposed that a disrupted modulation occurring in the sympathetic nervous system (SNS) plays an instrumental role in the onset of NMS. The said interruption leads to increased muscle tone and metabolism as well as unregulated vasomotor and sudomotor activity, which in turn results in ineffective heat dissipation as well as labile heart rate and blood pressure. In this model, the dopamine antagonists precipitate the symptoms by means of inducing a destabilizing effect in normal dopamine regulation by efferent sympathetic activity (ESA).

Familial clusters of this syndrome indicate a hereditary predisposition to the disease. Genetic studies have demonstrated the existence of a particular allele associated with a gene known as the dopamine D2 receptor is dominant in NMS patients. The allele in question is linked with decreased metabolism and dopaminergic activity as well as reduced function and density of dopamine receptors.

Symptoms

Symptoms become pronounced in the first two weeks of treatment in most patients, though may appear earlier or after several years.

The four characteristic symptoms typically develop over a number of days and often following the order illustrated below.

Altered mental status

A change in one’s mental status, such as an agitated delirium in most cases that may lead to reflecting encephalopathy (unresponsiveness) or lethargy, is typically acknowledged as the earliest manifestation.

Motor abnormalities

Patients may experience generalized forms of severe muscle rigidity, sometimes accompanied by tremors, resulting in cogwheel rigidity; or, less frequently, chorea, dystonias, or other abnormalities; and reflex responses are usually decreased

Hyperthermia

The body temperature of the patient is typically found to be higher than 38⁰C and often rises over 40⁰C

Autonomic hyperactivity

The is an increase in autonomic activity in the affected person that tends to cause arrhythmias, tachycardia, labile hypertension, and tachypnea

Diagnosis

The medical practitioner will search for the two primary symptoms, namely, stiff muscles and a high temperature. In addition to these, a number of other warning signs, such as high or low blood pressure, fast heartbeat, and sweating are also taken into account.

As a few other disorders mimic the symptoms that are identical to NMS, the specialist will perform any one or a combination of the following tests.

• Blood tests
• Urine tests
• Spinal fluid test
• Brain imaging scans
• Electroencephalogram (EEG) to trace electrical disturbances in the brain

Differential diagnosis

Infectious

• Meningitis or encephalitis
• Sepsis
• Brain abscess
• Rabies

Metabolic

• Rhabdomyolysis
• Acute renal failure (ARF)
• Pheochromocytoma
• Thyrotoxicosis

Environmental

• Spider envenomations
• Heat stroke

Drug-induced

• Malignant hyperthermia

Neuroleptic-induced

• Parkinsonism
• Acute akathisia
• Acute dystonia
• Postural tremor
• Tardive dyskinesia

Non-neuroleptic-induced

• Serotonin syndrome
• Monoamine oxidase inhibitor toxicity (MOIT)
• Anticholinergic delirium
• Lithium toxicity
• Strychnine poisoning
• Salicylate poisoning
• Drugs of abuse
• Cocaine
• Methamphetamine
• Amphetamine
• Phencyclidine
• 3,4-Methyl​enedioxy​methamphetamine (MDMA)

Drug-withdrawal syndrome

• Alcohol
• Baclofen
• Benzodiazepine
• Sedatives
• Hypnotics

Psychiatric or neurological

• Nonconvulsive status epilepticus (NSE)
• Parkinsonism
• Lethal catatonia

Autoimmune

• Polymyositis

Treatments

Initial Care

The general practitioner will first take the patient off the medication that triggered this syndrome. People with NMS receive treatment in an intensive critical care unit (ICCU) and the objective is remission of fever and providing the admitted individual with nutrition and fluids.

Medications

Medications used for treating this syndrome include muscle-relaxing agents like dantrolene and dopamine-boosting Parkinson’s disease drugs like bromocriptine or amantadine.

Electroconvulsive Therapy

If these medicines are found not to be useful, the doctor might go for electroconvulsive therapy (ECT), which is painless and applied when the patient is in slumber. A small amount of electrical impulse is sent to the brain to induce a seizure to relieve the sufferer from the symptoms.

Recovery & Relapse

NMS generally improves in a week to a fortnight, and after recovery, almost all the patients can return to their respective courses of antipsychotic drugs once again. The physician might recommend a different medication post-recovery from NMS.

This syndrome can make a comeback after treatment, and the doctor will carefully examine any warning signs that potentially indicate the recurrence. The longer a person waits to resume the course of antipsychotic medications, the less likely one acquires this syndrome again.

Prevention

Primary

• Administering the lowest effective quantity of antipsychotic medication
• Avoiding sudden increase in the dose of antipsychotic medicines, if possible
• Avoiding abrupt withdrawal of dopaminergic medication, especially in disorders like Parkinson’s disease where patients are compromised
• Treating agitation as early as possible and giving alternatives to antipsychotic drugs, whenever possible
• Avoiding dehydration

Secondary

• The use and amount of antipsychotic drugs should be reduced as much as possible, and agitation should be treated
• The application and dose of antipsychotic medication should be minimized and agitation treated.

Prognosis

Most episodes of this syndrome resolve within a fortnight. The mean recovery period reported is one two one-and-a-half week.  Some cases persist for half-a-year with motor signs and residual catatonia. It is also observed that risk factors are concomitant structural brain disease (CSBD) and depot antipsychotic use (DAPU) for an extended course. Most people are found to recover without developing neurologic sequelae, excluding the cases of severe hypoxia or when the body temperature is grossly elevated for a long time.

One to four in every twenty affected individuals succumb to this syndrome, and the manifestations of medical complications, as well as the severity of the disease, are considered as the most potential indicators of mortality. Patients with renal failure and myoglobinuria are found to have an increased mortality rate, which is estimated at one in every two NMS individuals. Higher mortality rates are also documented for lower-potency agents and typical antipsychotic drugs.

References

The post Neuroleptic Malignant Syndrome appeared first on All Health Site - Health Articles and News.

The mutant genes are transferred to the children in a process called the ADI or autosomal dominant inheritance. It indicated that only one copy of a mutated gene from the parent is required for the disease to appear in an individual. One in every two offspring of an affected person has the likelihood of one of them carrying the genetic variation, irrespective of whether one is male or female. At present, Brugada syndrome is estimated to be prevalent in one in every two thousand people.

Other Names of Brugada Syndrome

• Bangungut
• IVA
• Brugada type
• Pokkuri death syndrome (PDS)
• SUNDS
• SUDS

Causes

It is primarily caused by mutations affecting the SCN5A gene situated on chromosome three, and presently, over two hundred and fifty mutations are found to be associated with this syndrome reported in the following eighteen genes.

• SCN5A
• SCN1B
• SCN2B
• SCN3B
• SCN10A
• ABCC9
• GPD1L
• CACNA1C
• CACNB2
• CACNA2D1
• KCND3
• KCNE3
• KCNE1L -KCNE5-
• KCNJ8
• HCN4
• RANGRF
• SLMAP
• TRPM4

Symptoms

• Syncope and also cardiac arrest (happens during sleep or while resting in many patients)
• Nightmares or thrashing during night time
• Asymptomatic: However, a routine electrocardiogram does reveal ST-elevation in V1-V3

• Associated atrial fibrillation (AAF): Occurs in one in every five cases.
• Fever: Often reported to exacerbate or trigger clinical manifestations

The absence of a prodrome is found to be more typical for people with ventricular fibrillation documented, and this very absence is attributed to the onset of syncope in individuals with this syndrome.

Diagnosis

• Electrocardiogram (EKG or ECG): A medicine known as Flecainide or Ajmaline may be delivered intravenously during an electrocardiogram to watch how it affects the patient’s heart, and the attending doctor will look for the Brugada sign. However, not every affected individual exhibits this particular sign and such people may require multiple electrocardiograms at different times.
• Electrophysiology studies (EPS): It is typically done in CCL or cardiac catheterization laboratories.
• Blood tests for MGT or molecular genetic testing: Though DNA testing can be conducted for all genes to detect cases of mutation, only thirty to thirty-five in every hundred affected people carry an identifiable mutation in their genes. About twenty-five patients in every hundred are prescribed a sequential analysis to detect the faulty SCN5A gene in the initial stage of their genetic diagnosis.

Differential Diagnosis

• Pulmonary Embolism
• Hypothermia
• Acute Pericarditis

Treatments

The only proven and effective therapy is an ICD or implantable cardioverter that monitors one’s heart rhythm and sends electrical impulses on demand to regulate any abnormality in a heartbeat. Some doctors prescribe Quinidine where such implantations are not viable, for instance, in neonates.

An anti-arrhythmic agent like Isoproterenol is used in cases of UVA or unstable ventricular arrhythmias (bio-electrical storms). Recommendations to treat asymptomatic patients are controversial and possible therapies to evaluate the beneficiary for an ICD placement may include performing an EPS or electrophysiologic study, examining one’s family history, or putting the concerned individual under observation until the symptoms surface, though the first symptom happens to be an SCD or sudden cardiac death in some patients in the last case.

Genetic counseling is suggested for affected persons and their family members. Other treatments are supportive and symptomatic.

Prevention

One should always remember and attempt to avoid the following triggers for reducing the odds of having a fast heartbeat.

• High temperature (38⁰C) or fever: One should take paracetamol and seek professional advice as early as possible
• Consuming alcohol in an excessive amount: Binge drinking should be avoided
• Dehydration: A registered practitioner should be consulted in cases of persistent vomiting and diarrhea, and plenty of fluids, as well as special rehydration drinks, should be taken
• Certain Drugs: Avoiding any such medication that acts as a trigger for this syndrome

Prognosis

This syndrome can result in PVT or polymorphic ventricular tachycardia that may further degenerate, and lead to ventricular fibrillation, inducing cardiac arrest eventually. Prolonged hypoxia at the time of cardiac arrest may cause neurologic sequelae in such patients.

It is found that instances of ventricular fibrillation or sudden cardiac death occurred in eighty-two of every hundred patients diagnosed with this syndrome when a mean follow-up for two years is taken into account. A past history of syncope, a spontaneously atypical or abnormal electrocardiogram, and inducibility at the time of PES or programmed electrical stimulation (in one study) considerably increased this risk.

Aside from accidents, this syndrome may be one of the leading causes of death, in men who are less than forty years old. It is not possible to find out the true incidence because of the reporting biases. In spite of having a strong dependence for population, an estimated one in every twenty-five cases of sudden deaths, and also a minimum of one in every five incidents of sudden deaths observed in patients who have structurally normal hearts can be attributed to this syndrome. The mean age for the occurrence of sudden death is found to be twenty-six to fifty-six years for patients diagnosed with Brugada syndrome.

Brugada Syndrome Images

When to visit a doctor?

• If someone is experiencing arrhythmia (irregular heartbeat) or heart palpitations
• Facing unexplained seizures or blackouts
• Fainting
• If one’s child, parent, or sibling is diagnosed with this syndrome, the requirement for genetic testing for that individual may need to be evaluated thereafter by the general practitioner

If a close member of the family has a sudden death without any plausible cause, as this may potentially suggest the Brugada syndrome.

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SIDS is sudden infant death syndrome. It is the sudden and unexplained death of an infant below the age of one year. It is a very important thing to learn for all new parents as this death sleep which occurs suddenly between midnight and early morning without any signs of struggle or noise. In all such cases, the cause of the death remains unknown even after a detailed autopsy.

What Causes SIDS?

The exact cause is not known but there are many probable factors that are responsible for SIDS. These are sleeping on the stomach or baby sleeping on side, excessive bedding or toys in the crib, overheating, sudden exposure to smoke, tobacco smoke. Accidental suffocation can also be a resultant of bed sharing or co sleeping. Keeping the sleeping baby on the same cot as the parents is a very common practice in Asian countries but it is considered unsafe as deep sleepers or toddlers can be responsible for suffocating the baby. Another known risk factor is premature babies where the respiratory tract is still immature. SIDS is responsible for 80% of sudden infant deaths.

The demography of the syndrome shows that it is more common in developed countries and is seen more often in the babies below 6 months of age. It is more common in boys than in girls.

Risk Factors of SIDS

There are some risk factors that have been identified as potential causes of these sudden deaths in infants. They are:

1. Sleeping: Putting babies to sleep on their stomach is one of the important causes of SIDS. Presence of excessive bedding in the cot or soft toys can also prove risky as they can suffocate the baby. Before six months of age, babies are delicate and they cannot remove their arms or head from an odd position. They can turn but if they are getting suffocated in the face, they cannot help themselves. So it is said that babies under the age of one year should be made to sleep on their back with no toys or soft material in the cot.
2. Smoke: Infants who were exposed to smoke in uterus that is if the mother smoked during her pregnancy, then the chances of SIDS go up. Smoking is also associated with poor neural development in the baby.
3. Genetics: Male babies are 50% more prone to SIDS than females.
4. Bottle feeding: Parents who have a habit of giving the bottle in the bed to the baby are actually putting their kids at a big risk. If the baby falls asleep while drinking, the nipple may remain in the mouth and obstruct the breathing of the baby. This is an incorrect method of feeding and should be avoided.
5. Other Factors: There are other factors like drinking habit in parents which is found associated with SIDS to a great extent.

Prevention of SIDS

1. The most important rule in SIDS prevention is putting the baby to sleep on his back in baby crib. Some parents may be worried about their babies choking but putting them to bed on their tummy is a bigger risk.
2. The cot used for the baby should be firm with no extra pillows, bedding, newborn blankets or soft toys.
3. Smoke affects the health of the baby in a very big way. If you are smoking, ensure that you quit before you get pregnant. Second hand smoke is a very big risk factor for infant death syndrome.
4. Breastfeed your baby for as long as you can because the protective antibodies from the mother prevent infections in the baby which puts him at a risk for developing SIDS. If you are bottle feeding, never give the bottle to the child in bed. Feed him in your lap, burp him and then lay him down for sleep.
5. If you wish to keep your baby in the same room as yours, then use a co sleeper that gets attached to your bed. That way the baby is not at a risk of suffocation under the heavy bed blankets. When the baby is asleep put him in the bassinet (infant bed) next to you.
6. It is said that using a pacifier also reduces the risk of SIDS. When using one always remember that you should never put the pacifier in the mouth of a sleeping baby. Sterilize it properly and do not coat it with honey or any other substance.
7. Avoid hyperthermia and over heating of the baby. When putting him down, always wear loose and comfortable clothing. The best infant wear can be onesies which keeps the baby covered. Maintain the room temperature and avoid it from getting very hot or cold.
8. Never give honey to a baby under the age of one. It is associated with botulism and infections that can lead to SIDS.
9. There are products like cardiac monitors and respirators that claim to reduce the rate of SIDS. These products are mostly unnecessary and following the above tips will be sufficient to prevent SIDS in general.

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Euthyroid sick syndrome (ESS), also called non-thyroidal illness syndrome, is basically a self protective mechanism of the body, often occurring during a severe illness, or long starvation. It disrupts normal bodily functions, and is characterized by one or more typical hypothyroidism symptoms despite normal levels of thyroid stimulating hormones T3 and T4.

What Causes Euthyroid Sick Syndrome

The rare endocrine condition occurs when a chronic ailment or an insufficient intake of required calories produces stress in the body. Then, along with lowering of the hormone level, the body produces a type of thyroid hormone (reverse T3) so as to lessen the metabolic rate, which in turn decreases the damage brought by stress.

Risk Factors

ESS is more commonly reported in people with the following conditions:

• Sepsis
• Diabetic ketoacidosis
• Thermal injuries
• Chronic renal failure
• Cancer
• Protein deficiency
• A low carbohydrate diet or disorders in eating suggesting
• norexia nervosa
• Fasting
• Heart failure
• Pneumonia
• Cirrhosis

Newborns in intensive care units are also at a risk of getting affected by the condition.

Signs and Symptoms

The Euthyroid Sick Syndrome symptoms share a similarity with hypothyroidism and involve:

• Fatigue
• Weight gain
• Dry skin
• Depression
• Anxiety
• Low concentration
• Low libido
• Pain in muscles
• Hair loss

Euthyroid Sick Diagnosis and Tests

Blood tests are done to determine the level of TSH which may be low, normal or slightly elevated as compared to hypothyroidism in which the TSH level is usually high. These tests also help to detect an elevated serum cortisol levels.

Rarely, abnormal thyroid function test is done with severely ill patients to help in clinical judgment.

Differential Diagnosis:

• Hashimoto Thyroiditis
• Hyperthyroidism
• Hypothyroidism
• Thyroid Dysfunction
• Hypopituitarism

Treatment and Management

Since the hormone levels generally become normal with proper treatment of the underlying ailment, there are no special treatment measures for ESS. Some therapies and medicines that may help to improve the symptoms include:

• Short term specific thyroid medication, such as amiodarone, and corticosteroids
• Intravenous vitamin therapy or administration of important vitamins and minerals through the veins
• Message therapy (for pain and stress associated with the syndrome)

The other modes of treatment and management options are supplements to manage adrenaline function and stress, acupuncture, and changes in lifestyle.

Prevalence and Incidence

ESS can affect people irrespective of age and sex. Its incidence rate is about 70% in hospital inpatients and 10% among hospitalized patients with lower TSH.

Prognosis

Recovery is based on the stage of the underlying illness. Most patients recover with successful treatment of the underlying non-thyroidal ailment, but excessively lowered levels of T4, along with an acute sickness is associated with the risk of mortality.

Euthyroid Sick Syndrome ICD-9-CM and ICD-10 Codes

The ICD-9-CM code for the syndrome is 790.94, and the ICD-10 code is E07.8.

References:

1. http://my.clevelandclinic.org
2. http://www.mountsinai.org
3. http://en.biomanantial.com
4. http://circ.ahajournals.org
5. http://www.fmdsa.org

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Lennox Gastaut Syndrome (LGS), also called childhood epileptic encephalopathy, is a rare severe form of progressive epilepsy, characterized by multiple types of seizures that are most prominent during infancy or early childhood (age 3-8 years), but may persist through adolescence to adult years. Affected children may also have intellectual functioning impaired as well as face behavioral problems and delayed development.

The disorder, first discovered by Tissot in 1770, can be classified into two types on the basis of the cause of the symptoms:

• Symptomatic LGS
• Cryptogenic or Idiopathic LGS

Lennox Gastaut Syndrome Symptoms

Symptoms consist of different types of seizures and neurological malfunctions. Amidst the seizures, the more common are the tonic and atonic or “drop” seizures.

Tonic Seizures, affecting about 74-90% of children with LGS are brief, occur mostly at night and can be triggered by noise, contact or movement. They may cause:

• A slight bending of the body inward due to muscle contractions
• Brief holding of breath
• The opening of mouth and rolling of eyes
• Abnormal rise of upper arms and legs much like a ballet dancer
• Sudden collapse of the affected individual due to short loss of consciousness

Atonic Seizures, also lasting for a minute time are characterized by:

• Dropping of eyelids and nodding of head
• Sudden falls
• A tendency to collapse forward or backward particularly at the waist
• Brief consciousness loss
• Jerking muscle movements

Atypical Absence Seizures, which are abrupt, are characterized by:

• A span of unconsciousness
• Unresponsive staring
• Confusion
• Twitching around eyes or mouth
• Stiffening of neck
• Drooping of head and body

Less common forms of seizures occurring in the condition include myoclonic, tonic-clonic, status epilepticus and nonconvulsive status epilepticus seizures.

The less frequent neurological symptoms that generally develop with time involve:

• Difficulty in sitting, crawling or walking suggesting delayed motor development
• Loss of previously learned skills
• Hyperactivity, aggressiveness and a tendency to seek attention suggesting behavioral problems
• A slowing down of thought with reduced physical movement indicating psychomotor regression

Complications

• Drop seizures replaced by partial seizures and secondarily generalized convulsions
• Acute psychotic episodes
• Chronic psychosis
• Autism
• Perseverance
• Apathy
• Mental retardation
• Cognitive incapability involving slowness in response and information processing
• ADHD
• Head injuries and even death from fall or seizure
• Renal, cardiac or metabolic complications
• Cerebral palsy
• Blindness
• Hearing loss

What Causes Lennox Gastaut Syndrome

The reasons behind Symptomatic Lennox-Gastaut syndrome, which accounts for nearly 70-80% of cases, are:

• Internal injuries of brain resulted from problems before, at or during birth such as prematurity, insufficient supply of oxygen called perinatal hypoxia and low birth weight
• Abnormal brain cortex development suggesting cortical dysplasia
• Stroke
• Trauma
• Severe brain infections such as encephalitis or meningitis
• A rare genetic disorder known as tuberous sclerosis
• Degenerative or metabolic nervous system disorders

Cryptogenic LGS which does not have an identifiable cause may have a later onset. **

Although in most cases, the causes are identifiable, yet the exact mechanisms that bring about the seizures are not known, and more researches need to be done to derive a genetic basis of the syndrome.

Risk Factors

• Family history of epilepsy
• West syndrome

Lennox Gastaut Syndrome Tests and Diagnosis

The diagnosis of LGS is based on the identification of the clinical triad that comprises of multiple seizures, an abnormal EEG with a significant spike-wave pattern of the brain and some degree of cognitive and behavioral dysfunction. An advanced imaging technique such as MRI is also done to get three-dimensional images of the brain anatomy.

Differential Diagnosis

• Early onset childhood absence epilepsy
• Dravet syndrome
• Atypical benign partial epilepsy
• Myoclonic astatic epilepsy

Treatment and Management

Administration of Anti-Epileptic Drugs (AEDs)

Treatment may start with medications, which often include:

• Valproate, which may be given alone or in combination with other drugs like lamotrigine, topiramate or clobazam. Though valproate is beneficial for all types of seizures, yet it has side effects such as tremors or reduction in platelet counts.
• Another drug of choice, topiramate may help lessen both drop attacks and multiple seizures but an increased dose can have side effects like sleepiness and ataxia.
• Clonazepam, the most commonly used representative of the benzodiazepine class of drugs may have partial effect in myoclonic seizures.
• Lamotrigine seems to be efficient in multiple seizures as well as a mood stabilizer.
• Felbamate may help promote alertness, but it too can induce aplastic anemia.
• FDA has approved Levetiracetam for partial seizures, but it may prove efficient in other seizures too.
• Rufinamide (Benzel) is used as an adjunctive therapy for adults and children aged one or above having seizures.

Rehabilitation Programs

Occupational therapy, speech and physical therapy are the rehabilitation procedures that may help children suffering from the syndrome in reducing the levels of disability.

The Ketogenic Diet

However, since the above mentioned drugs may lose their effect with the passage of time, the condition may be treated with the help of another approach called the ketogenic diet. This strict high fat, low carbohydrate diet is initiated after a 24-hour fasting, intending to raise the ketone level in the brain. By restricting an intake of carbohydrates, this diet forces the body to burn fat to get energy instead of sugar. Followed under the strict supervision of a doctor and dietician, it does not prevent the use of medications. Vitamins and minerals may be supplemented to avoid a deficiency. Though proving effective in a minority of patients, it may have side effects like dehydration, constipation, kidney stones and vomiting.

Surgical Therapies  – Lennox Gastaut Syndrome

Corpus Callosotomy

Patients not responding to either medications or dietary therapy undergo a surgical procedure called corpus callosotomy. This surgery, accomplished by cutting the large bundle of nerve fibers called the corpus callosum that connects the two hemispheres is done to reduce the severity of drop attacks, tonic, and tonic-clonic seizures.

According to several studies, in 50- 70% of cases, partial callosotomy is beneficial whereas complete callosotomy may result in the decrease of drop attacks in about 80-90% of cases.

Vagus Nerve Stimulator

This surgery lasting for about an hour and usually conducted under anesthesia, involves the insertion of a device called a pulse generator into the chest to transmit mild, electrical impulses to the brain through the vagus nerve. This process, intending to reduce the frequency of the seizures may have side effects such as voice hoarseness, tickling in the throat and coughing.

The other surgical procedures are RNS stimulator, deep brain stimulation, and trigeminal nerve stimulation.

Treatment Through Nonpharmacological Means Include

• Intravenous Immunoglobulin (IVIG): IVIS is a blood product that can be given intravenously in the treatment of LGS.
• Medical Marijuana/CBD (Cannabidiol): A compound called cannabidiol found in cannabis might reduce chemical as well as electrical activity that occurs in the brain and thus may be used therapeutically for patients living with LGS.

Prevalence

The annual incidence of children having LGS is about 2 per 1000,000 children. Nearly 1-2% of all childhood epilepsies are represented by LGS. Amidst this, 75-90% children suffer from mental retardation which generally begins within a few years of the onset of the syndrome.

Prognosis and Life Expectancy

The prognosis of this progressive syndrome varies with individuals. Seizures continue in more than 80% of patients. MRIs and other clinical exams may occasionally be repeated to look for any change in the brain. The mortality rate of the syndrome ranges from 3% to 7% with most of the deaths occurring from accidents. The degree of disability may be lessened with early and useful treatment. Recovery also depends on the combined efforts of health care providers such as social workers and neuropsychologists.

ICD Code- 9 and ICD Code- 10

The icd-9 code for LGS is 345.0 and the ICD- 10 Code is G40.814.

References:

1. http://www.orpha.net
2. http://www.childneurologyfoundation.org
3. http://patient.info
4. http://www.aboutkidshealth.ca
5. https://www.epilepsy.org
6. http://www.lgsfoundation.org

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HIV is a commonly heard word these days. However, it is very important to understand what is HIV and what is AIDS. Acquired Immunodeficiency Syndrome (AIDS) is the disease which is caused by Human Immunodeficiency Virus (HIV). This virus attacks the CD4 cells commonly called as T cells which are a part of our body’s immune system. The defense mechanism provides immunity and performs the major function of protecting the body from infections by fighting off the bacteria and viruses. This immune system gradually gets affected and the person becomes susceptible to even minor infections. The immunity level of the affected individual decreases further as the disease progresses.

Transmission of HIV

The HIV Virus is found in the body fluids and blood of the affected person. It is present in blood, semen, vaginal fluid and even breast milk. So the disease is transmitted by blood to blood contact or sexual contact.

• Pregnant ladies with HIV infection can pass it on to the unborn baby during delivery or through the breast milk.
• Other common modes of transmission include use of infected needles and syringes which contain blood traces of an infected person.
• Sexual contact in the form of oral sex, vaginal and anal sex
• Through blood transfusion.
• Sharing of infected needles by intravenous drug users.

Symptoms of HIV

AIDS symptoms or HIV symptoms can be better understood if we get an idea about the different stages of the disease.

Stage 1: Acute Infection

After an exposure to the HIV virus, the person is asymptomatic for the first 2-4 weeks which is the incubation period. At this stage, the person is highly infectious but unaware of the disease. He experiences mild flu like symptoms as follows which may continue over a few weeks.

• Fever
• Chills
• Joint pain
• Sore throat
• Night sweats
• Tiredness and weakness
• Skin rashes (HIV Rash)

Stage 2: Asymptomatic Infection

After the initial symptoms regress, there is a stage of clinical latency where the virus continues to grow and multiply but since there are no symptoms, the person feels normal. However he is highly contagious. If no treatment is given, this stage can last up to a decade which will end into a fully blown picture of AIDS.

If the diagnosis is made in time and the person is put on ART, then this stage can be prolonged for a few decades. But AIDS is a lifelong disease as there is no cure for HIV. The person has to live with it till the end.

Stage 3: Acquired Immunodeficiency Syndrome

A fully blown picture of AIDS is the most severe form of HIV infection. The person diagnosed at this stage will not be able to live for more than 3 years. The immune system is damaged and the person is very susceptible to even minor infections. Common HIV AIDS symptoms seen during this stage are:

• Fever lasting for weeks
• Long standing chronic diarrhea
• Night sweats
• Permanent tiredness
• Enlarged lymph nodes
• Weight loss
• White spots on the tongue

Diagnosis and Treatment of HIV

HIV Test: HIV blood test by ELISA is the commonest diagnostic test and is done in case there is a history of exposure. The results of the test may be negative initially and can take up to three months to get a HIV positive result.

CD4 and CD8 count are done to get an idea about the immunity status. Low CD4 count indicates advanced stage of AIDS.

Treatment is mainly done by Anti-Retroviral Drugs (ARTs). The main aim of treatment is to reduce the viral load and maintain a high CD4 count so that the person is immunologically capable of carrying out his day to day activities. HIV patients are however very susceptible to infections, tuberculosis being the commonest one of all other infections.

Scientists are working on developing a HIV vaccine which is challenging as the virus is highly mutable and adapts as soon as HIV antibodies are introduced.

Prevention of HIV

1. Use of a condom can prevent the spread of HIV. Unprotected sex puts one at a risk for contracting HIV and other sexually transmitted diseases.
2. Sharing needles by intravenous drug users also leads to spread of the disease. Awareness in this matter will prove beneficial.
3. Medical and paramedical staff should take adequate care by using gloves to avoid contact with contaminated blood and body fluids of patients.
4. All pregnant ladies should be screened for HIV as it is transmitted to the unborn child. An effective treatment plan like planned cesarean, bottle feeding etc can help if the mother is found infected.
5. Health and sex education to teenagers should be imparted in all schools to make them aware of the disease.

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