The CDC describes the effects of eating toxic blowfish thusly: First stage: Numbness and sensation of prickling and tingling (paresthesia) of the lips and tongue, followed by facial and extremity paresthesias and numbness, headache, sensations of lightness or floating, profuse sweating (diaphoresis), dizziness, salivation (ptyalism), nausea, vomiting (emesis), diarrhea, abdominal (epigastric) pain, difficulty moving (motor dysfunction), weakness (malaise), and speech difficulties.
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There may be an association between widespread fasciculations or paresthesias with small fiber neuropathy.
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Case reports have shown that overdoses with 4-AP can lead to paresthesias, seizures, and atrial fibrillation.
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People may experience numbness, prickling or tingling sensations (paresthesias), or the feeling a limb has "fallen asleep" (an indicator of nerve compression), burning, cutting or other sensations.
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Wartenberg's migratory sensory neuropathy (also known as Wartenberg's migrant sensory neuritis) affects the cutaneous nerves. A benign, relapsing and remitting condition involving pain, numbness and paresthesias in the sensory and peripheral nerves.
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Convulsive symptoms of ergotism Convulsive symptoms include painful seizures and spasms, diarrhea, paresthesias, itching, mental effects including mania or psychosis, headaches, nausea and vomiting. Usually the gastrointestinal effects precede central nervous system effects.
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Neuro-ophthalmic examinations reveal pupillary defects (e.g. Marcus Gunn Pupil). Funduscopic examinations, examinations of the fundus of the eye, allow detection of arteriovenous malformations. Neurological examination can determine neurological deficits such as hemiparesis and paresthesias.
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These can sometimes be painful with paresthesias and dysesthesias.Yuebing L, Lederman RJ. Sural mononeuropathy: A report of 36 cases. Muscle Nerve 49:443-445, 2014. Nerve conduction studies can be used to delineate sural nerve lesions.
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The differential diagnosis of patients who experience symptoms of paresthesias, derealization, dizziness, chest pain, tremors, and palpitations can be quite challenging.Sudden Onset Panic: Epileptic Aura or Panic Disorder? Robin A. Hurley, M.D., Ronald Fisher, M.D., Ph.D. and Katherine H. Taber, Ph.D.
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Atlantoaxial instability is a common asymptomatic finding in rheumatoid arthritis patients. However, it can lead to cervical myelopathy. Patients with atlantoaxial instability can experience neck pain and headaches in the back of the head (occipital headaches). Myelopathic symptoms include: weakness, gait disturbance, paresthesias, and loss of dexterity (e.g.
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The other affects middle-aged and elderly people. They suffer sensory polyneuropathy, including weakness and paresthesic sensations. Paresthesias include sensations of numbness, heat, cold, tightness, crawling motion, tingling, pins and needles, and a feeling of walking on cotton or pebbles. Weaknesses show as gait ataxia (lack of co-ordination).
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Clinical Features The signs and symptoms of DIAM are similar to infectious meningitis including but not limited to headache, fever, neck stiffness, altered mental status and other neurological deficits such as numbness, paresthesias, seizure or weakness. Notably, the patient will have had recent exposure to one of the causative medications.
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These crises are characterized by porphyria. They typically follow an infection. Patients can present with a variety of varied symptoms including paresthesias, abdominal pain, pain-induced seizures, and can result in self-mutilation in response to this pain. Episodes can last for 1–7 days and can lead to neuropathy.
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Numbness and paresthesias in the median nerve distribution are the hallmark neuropathic symptoms (NS) of carpal tunnel entrapment syndrome. Weakness and atrophy of the thumb muscles may occur if the condition remains untreated, because the muscles are not receiving sufficient nerve stimulation. Discomfort is usually worse at night and in the morning.
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Neurogenic claudication describes pain, weakness, fatigue, and/or paresthesias that extend into the lower extremities. These symptoms may involve only one leg, but they usually involve both. Leg pain is usually more significant than back pain in individuals who have both. is classically distinguished by symptoms improving or worsening with certain activities and maneuvers.
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These systemic effects are caused by a traumatic rhabdomyolysis. As muscle cells die, they absorb sodium, water and calcium; the rhabdomyolysis releases potassium, myoglobin, phosphate, thromboplastin, creatine and creatine kinase. Crush syndrome can directly come from compartment syndrome, if the injury is left untreated. Monitor for the classic 5 Ps: pain, pallor, paresthesias (pins and needles), paralysis, and pulselessness.
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CMV polyradiculomyelopathy (PRAM) is one of the five distinct neurological syndromes caused by CMV in HIV/AIDS. It causes subacute ascending lower extremity weakness with paresthesias and radicular pain, hyporeflexia or areflexia, and urinary retention. It has been suggested that CMV polyradiculomyelopathy should be treated with both ganciclovir and foscarnet in patients who develop the disease while taking either of these drugs.
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Improper reinsertion of donor site muscles on the iliac crest can cause postoperative complications, like a hernia. Also, nerve paresthesias are possible. ;Indication The Rubens flap is indicated if a TRAM flap is not possible because of a previous abdominal surgery or if the patient does not accept an abdominal scar. ;Contraindication Insufficient skin and fat redundancy at donor site.
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Patients (77% female; median age 55 years, ranging from 18 to 78 years) presented with various neurological signs and symptoms depending on the site of involvement. The most common presenting symptoms were headache (30 cases); seizures (22 cases); and visual changes (19 cases). Less commonly, patients presented with paresthesias (i.e. abnormal skin sensations), motor deficits, and ataxias, memory failures, and dizziness.
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Abnormalities in neuronal excitability have been noted in amyotrophic lateral sclerosis and diabetes patients. While the mechanism ultimately responsible for the variance differs between the two conditions, tests through a response to ischemia indicate a similar resistance, ironically, to ischemia and resulting paresthesias. As ischemia occurs through inhibition of the sodium-potassium pump, abnormalities in the threshold potential are hence implicated.
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The tumor must be removed with as complete a surgical excision as possible. In nearly all cases, the ossicular chain must be included if recurrences are to be avoided. Due to the anatomic site of involvement, facial nerve paralysis and/or paresthesias may be seen or develop; this is probably due to mass effect rather than nerve invasion. In a few cases, reconstructive surgery may be required.
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Oral or intravenous harmine doses ranging from 30–300 mg may cause agitation, bradycardia or tachycardia, blurred vision, hypotension, paresthesias. Serum or plasma harmine concentrations may be measured as a confirmation of diagnosis. The plasma elimination half-life is on the order of 1–3 hours.R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 727-728.
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Symptoms of a sprain or tear of the LCL includes pain to the lateral aspect of the knee, instability of the knee when walking, swelling and ecchymosis (bruising) at the site of trauma. Direct trauma to the medial aspect of the knee may also affect the peroneal nerve, which could result in a foot drop or paresthesias below the knee which could present itself as a tingling sensation.
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The three doctors noticed that two soldiers, who were suffering from muscular weakening and pain along with paresthesias,Guillain–Barré–Strohl syndrome at Who Named It had an unexpected amount of spinal fluid protein production.Guillain–Barré syndrome by Wilder D. Smith American Chemical Society, 2002, diseasesanddisorders. Strohl is credited with performing the electrophysiological tests on the soldiers. Eventually, the two patients were able to recover from their illness.
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Formication is the sensation that resembles that of small insects crawling on (or under) the skin when there is nothing there. It is one specific form of a set of sensations known as paresthesias, which also include the more common prickling, tingling sensation known as "pins and needles". Formication is a well documented symptom, which has numerous possible causes. The word is derived from formica, the Latin word for ant.
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The symptoms of sedative/hypnotic toxidrome include ataxia, blurred vision, coma, confusion, delirium, deterioration of central nervous system functions, diplopia, dysesthesias, hallucinations, nystagmus, paresthesias, sedation, slurred speech, and stupor. Apnea is a potential complication. Substances that may cause this toxidrome include anticonvulsants, barbiturates, benzodiazepines, gamma-Hydroxybutyric acid, Methaqualone, and ethanol. While most sedative-hypnotics are anticonvulsant, some such as GHB and methaqualone instead lower the seizure threshold, and so can cause paradoxical seizures in overdose.
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Paresthesia is an abnormal sensation of the skin (tingling, pricking, chilling, burning, numbness) with no apparent physical cause. Paresthesia may be transient or chronic, and may have any of dozens of possible underlying causes. Paresthesias are usually painless and can occur anywhere on the body, but most commonly occur in the arms and legs. The most familiar kind of paresthesia is the sensation known as "pins and needles" after having a limb 'fall asleep'.
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The middle cerebral artery is most often affected. Parenchymal syphilis occurs years to decades after initial infection. It presents with the constellation of symptoms known as tabes dorsalis, because of a degenerative process of the posterior columns of the spinal cord. The constellation includes Argyll Robertson pupil, ataxic wide- based gait, paresthesias, bowel or bladder incontinence, loss of position and vibratory sense, loss of deep pain and temperature sensation, acute episodic gastrointestinal pain, Charcot joints, and general paresis.
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Reported symptoms of overexposure affect the nervous system and include confusion, slurred speech, dizziness, paresthesias, and difficulty walking, unusual fatigue and headaches, development of arthralgias, visual disturbances (difficulty focusing), and muscle twitching. Symptoms may persist over one year. Other symptoms include irritation of mucous membranes, eyes, upper respiratory tract, and skin, as well as transient loss of consciousness. Loss of feeling in the feet, an example of paresthesia, is colloquially called "dead foot" by workers who suffer from it.
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When in the dry form the patient experience pains in their extremities, paresthesias, paralyses, and contractures due to being a paralytic type of disease. When beriberi is in its wet form the patient can expect swelling of the extremities and face along with an effusion of fluid into their joints, pleural cavity, and pericardial cavity. Beriberi in this form can lead to sudden death. New England fishermen first discovered the disease in Colonial America in the 19th century.
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Subclavian steal syndrome arises from retrograde (reversed) flow of blood in the vertebral artery or the internal thoracic artery, due to a proximal stenosis (narrowing) and/or occlusion of the subclavian artery. Symptoms such as syncope, lightheadedness, and paresthesias occur while exercising the arm on the affected side (most commonly the left). Aortic dissection (a tear in the aorta) and cardiomyopathy can also result in syncope. Various medications, such as beta blockers, may cause bradycardia induced syncope.
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Specifically, IFRA recommends that leave-on skin products be limited to 0.4% bergamot oil, which is more restrictive than any other Citrus-based essential oil. Although generally recognized as safe for human consumption, bergamot essential oil contains a significant amount of bergamottin, one of two furanocoumarins believed to be responsible for a number of grapefruit–drug interactions. In one case study, a patient who consumed four liters of Earl Grey tea per day suffered paresthesias, fasciculations and muscle cramps.
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Injury to the median nerve proper occurs in 0.06% of cases. Risk of nerve injury has been found to be higher in patients undergoing endoscopic CTR compared with open, though most are temporary neurapraxias. The palmar cutaneous branch of the median nerve may be injured during superficial skin dissection or while releasing the proximal portion of the transverse carpal ligament with scissors or an endoscopic device. Nerve injury can lead to persistent paresthesias or painful neuroma formation.
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During marketing of other SSRIs and SNRIs, there have been spontaneous reports of adverse events occurring upon discontinuation of these drugs, particularly when abrupt, including the following: dysphoric mood, irritability, agitation, dizziness, sensory disturbances (e.g., paresthesias such as brain zap electric shock sensations), anxiety, confusion, headache, lethargy, emotional lability, insomnia, hypomania, tinnitus, and seizures. The withdrawal syndrome from duloxetine resembles the SSRI discontinuation syndrome. When discontinuing treatment with duloxetine, the manufacturer recommends a gradual reduction in the dose, rather than abrupt cessation, whenever possible.
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Paresthesias of the hands, feet, legs and arms are common, transient symptoms. The briefest, electric shock type of paresthesia can be caused by tweaking the ulnar nerve near the elbow. Similar brief shocks can be experienced when any other nerve is tweaked (a tweaked neck nerve may cause a brief shock-like paresthesia toward the scalp). In the older age group, spinal column irregularities may tweak the spinal cord briefly when the head or back is turned, flexed, or extended into brief uncommon positions (Lhermitte's sign).
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After recovery from a primary herpes infection, the virus is not cleared from the body, but rather lies dormant in a non- replicating state within the trigeminal ganglion. Herpes Labialis may follow from primary herpes infection/herpetic gingivostomatitis The trigeminal ganglion is damaged, by infection or surgery, in Trigeminal trophic syndrome. Trigeminal trophic syndrome causes paresthesias and anesthesia, which may lead to erosions of the nasal ala. The thermocoagulation or injection of glycerol into the trigeminal ganglion has been used in the treatment of trigeminal neuralgia.
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Bourne, E. (2005). The Anxiety and Phobia Workbook, 4th Edition: New Harbinger Press. A panic attack can result when up-regulation by the sympathetic nervous system (SNS) is not moderated by the parasympathetic nervous system (PNS). The most common symptoms include trembling, dyspnea (shortness of breath), heart palpitations, chest pain (or chest tightness), hot flashes, cold flashes, burning sensations (particularly in the facial or neck area), sweating, nausea, dizziness (or slight vertigo), light-headedness, heavy-headedness, hyperventilation, paresthesias (tingling sensations), sensations of choking or smothering, difficulty moving, and derealization.
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PAAs are most often asymptomatic. Chronic symptoms are most often secondary to the mass effect exerted upon adjoining structures by the aneurysm (e.g. pain and paresthesias due to tibial nerve compression, calf swelling due to compression of the popliteal vein). Thrombosis within the aneurysm and subsequent luminal narrowing may result in claudication of gradual onset, while an acute thrombosis (occluding the vessel at the side of the aneurysm or lodging distally as the vessel narrows) may lead to acute lower extremity ischaemia and associated symptomatology (pain, paresthesia, paresis, pallor, poikilothermia).
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Diffuse tightness and tenderness over the entire belly of the tibialis anterior muscle that does not respond to elevation or pain medication can be early warning signs and suggestive of Anterior Compartment Syndrome. Other common symptoms include excessive swelling that causes the skin to become hot, stretched and glossy. Pain, paresthesias, and tenderness in both the ischemic muscles and the region supplied by the deep common fibular nerve are exhibited by patients suffering from this condition. Sensitivity to passive stretch and active contraction are common, and tend to increase the symptoms.
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Mulder's Sign is a physical exam finding associated with Morton's neuroma, which may be elicited while the patient is in the supine position on the examination table. The pain of the neuroma, as well as a click, can be produced by squeezing the two metatarsal heads together with one hand, while concomitantly putting pressure on the interdigital space with the other hand. With this technique, the pain of the Morton's neuroma will be localized strictly to the plantar surface of the involved interspace, with paresthesias radiating into the affected toes.
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Benign paroxysmal vertigo of childhood is an example of migraine-associated vertigo in which headache does not often occur. Basilar artery migraine (BAM) consists of two or more symptoms (vertigo, tinnitus, decreased hearing, ataxia, dysarthria, visual symptoms in both hemifields or both eyes, diplopia, bilateral paresthesias, paresis, decreased consciousness and/or loss of consciousness) followed by throbbing headache. Auditory symptoms are rare. However, a study showed a fluctuating low-tone sensorineural hearing loss in more than 50% of patients with BAM with a noticeable change in hearing just before the onset of a migraine headache.
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For the treatment of tuberculosis, cycloserine is classified as a second-line drug, i.e. its use is only considered if one or more first-line drugs cannot be used. Hence, cycloserine is restricted for use only against multiple drug-resistant and extensively drug-resistant strains of M. tuberculosis. Another reason for limited use of this drug is the neurological side effects it causes, since it is able to penetrate into the central nervous system (CNS) and cause headaches, drowsiness, depression, dizziness, vertigo, confusion, paresthesias, dysarthria, hyperirritability, psychosis, convulsions, and shaking (tremors).
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Alcoholic polyneuropathy usually has a gradual onset over months or even years although axonal degeneration often begins before an individual experiences any symptoms. An early warning sign (prodrome) of the possibility of developing alcoholic polyneuropathy, especially in a chronic alcoholic, would be weight loss because this usually signifies a nutritional deficiency that can lead to the development of the disease. The disease typically involves sensory and motor loss, as well as painful physical perceptions (paresthesias), though all sensory modalities may be involved. Symptoms that affect the sensory and motor systems seem to develop symmetrically.
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Though Kellogg stated that "electricity is not capable of accomplishing half the marvels that are claimed for it by many enthusiastic electrotherapists," he still believed electric currents to be "an extremely valuable therapeutic agent, especially when utilized in connection with hydrotherapy, thermotherapy, and other physiologic methods." Full text at Internet Archive (archive.org) As a result, electrotherapy coils were used in the Static Electrical Department of the Battle Creek Sanitarium especially for cases of paresthesias of neurasthenia, insomnia, and certain forms of neuralgia. Devices were also utilized to administer electric shocks to various parts of a patient's body.
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To date, reported adverse events and side effects have been mild to moderate. Possible adverse events include gait difficulties, balance disturbances, paresthesias, headache, skin burns with ulcerations, skin retraction, scars, and blood clots. This procedure is contraindicated in pregnant women, persons who have non-MRI compatible implanted metallic devices, allergy to MR contrast agents, cerebrovascular disease, abnormal bleeding, hemorrhage and/or blood clotting disorders, advanced kidney disease or on dialysis, heart conditions, severe hypertension, and ethanol or substance abuse, among others. The US Food and Drug Administration (FDA) approved Insightec’s Exablate Neuro system to treat essential tremor in 2016.
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Serotonin reuptake inhibitors should not be abruptly discontinued after extended therapy, and whenever possible, should be tapered over several weeks to minimize discontinuation-related symptoms which may include nausea, headache, dizziness, chills, body aches, paresthesias, insomnia, and brain zaps. Paroxetine may produce discontinuation-related symptoms at a greater rate than other SSRIs, though qualitatively similar effects have been reported for all SSRIs. Discontinuation effects appear to be less for fluoxetine, perhaps owing to its long half-life and the natural tapering effect associated with its slow clearance from the body. One strategy for minimizing SSRI discontinuation symptoms is to switch the patient to fluoxetine and then taper and discontinue the fluoxetine.
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Several different malignancies, particularly small-cell lung cancer and Hodgkin lymphoma, are associated with a paraneoplastic neuritis. This carcinomatous polyneuropathy is associated with the presence of antibodies against onconeural antigen, Hu, Yo, amphiphysin, or CV2/CRMP5, which recognize and bind to both tumor cells and peripheral nervous system neurons. This paraneoplastic syndrome may present as either a sensory neuropathy, affecting primarily the dorsal root ganglion, resulting in a progressive sensory loss associated with painful paresthesias of the upper limbs, or a mixed sensorimotor neuropathy which is also characterized by progressive weakness. Treatment of paraneoplastic syndromes aim for both elimination of tumor tissue via conventional oncologic approach as well as immunotherapy options such as steroids, plasmapheresis or IVIG.
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Because of this, people with Bell's palsy may present with loss of taste sensation in the anterior 2/3 of the tongue on the affected side. Although the facial nerve innervates the stapedius muscle of the middle ear (through the tympanic branch), sound sensitivity, causing normal sounds to be perceived as very loud, (hyperacusis), and dysacusis are possible but hardly ever clinically evident. Although defined as a mononeuritis (involving only one nerve), people diagnosed with Bell's palsy may have "myriad neurological symptoms" including "facial tingling, moderate or severe headache/neck pain, memory problems, balance problems, ipsilateral limb paresthesias, ipsilateral limb weakness, and a sense of clumsiness" that are "unexplained by facial nerve dysfunction".
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Deficiency of magnesium can cause tiredness, generalized weakness, muscle cramps, abnormal heart rhythms, increased irritability of the nervous system with tremors, paresthesias, palpitations, low potassium levels in the blood, hypoparathyroidism which might result in low calcium levels in the blood, chondrocalcinosis, spasticity and tetany, migraines, epileptic seizures, basal ganglia calcifications and in extreme and prolonged cases coma, intellectual disability or death. Magnesium plays an important role in carbohydrate metabolism and its deficiency may worsen insulin resistance, a condition that often precedes diabetes, or may be a consequence of insulin resistance. People being treated on an intensive care unit (ICU) who have a low magnesium level may have a higher risk of requiring mechanical ventilation, and death.
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Common side effects include diarrhea, nausea, vomiting, mild rashes, asymptomatic elevations in liver enzymes, and fever. Uncommon side effects include fatigue and malaise, behavioral changes, paresthesias and seizures, muscle cramps, and nose bleeds. Rare (may affect up to 1 in 10,000 people taking montelukast) but serious side effects include behavioral changes (including suicidal thoughts), angioedema, erythema multiforme, and liver problems. In 2019 and 2020, concerns for neuropsychiatric reactions were added to the label in the United Kingdom and United States where the most frequently suspected were nightmares, depression, insomnia (may affect between 1 in 100 to 1 in 1,000 people taking montelukast); aggression, anxiety and abnormal behaviour or changes in behaviour (may affect between 1 in 1,000 to 1 in 10,000 people taking montelukast).
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The neurological complex, defined as myelosis funicularis, consists of the following symptoms: # Impaired perception of deep touch, pressure and vibration, loss of sense of touch, very annoying and persistent paresthesias # Ataxia of dorsal column type # Decrease or loss of deep muscle-tendon reflexes # Pathological reflexesBabinski, Rossolimo and others, also severe paresis Vitamin B12 deficiency can cause severe and irreversible damage, especially to the brain and nervous system. These symptoms of neuronal damage may not reverse after correction of blood abnormalities, and the chance of complete reversal decreases with the length of time the neurological symptoms have been present. Elderly people are at an even higher risk of this type of damage. In babies a number of neurological symptoms can be evident due to malnutrition or pernicious anemia in the mother.
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Symptoms of exposure to this type of compound include cholinesterase inhibition, miosis, frontal headache, increased bronchial secretion, nausea, vomiting, sweating, abdominal cramps, diarrhea, lacrimation, increased salivation, bradycardia, cyanosis and muscular twitching of the eyelids, tongue, face and neck, possibly progressing to convulsions. Other symptoms include hyperemia of the conjunctiva, dimness of vision, rhinorrhea, bronchoconstriction, cough, fasciculation, anorexia, incontinence, eye changes, weakness, dyspnea, bronchospasm, hypotension or hypertension due to asphyxia, restlessness, anxiety, dizziness, drowsiness, tremor, ataxia, depression, confusion, neuropathy (rare), coma and death from depression of respiratory or cardiovascular systems. Exposure to this type of compound may result in giddiness, nervousness, blurred vision, discomfort (tightness) in chest, papilledema, muscular weakness, loss of reflexes, loss of sphincter control, cardiac arrhythmias, various degrees of heart block and cardiac arrest. It may also result in spasm of accommodation, aching pain in and about the eye, nystagmus, delayed distal axonopathy and paresthesias and paralysis of limbs.
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A 2008 paper presented a study of 116 cases, observed over 36 years. The authors looked at the family trees of people with MMND, and found evidence for autosomal recessive inheritance in 15 of the 16 families studied, and autosomal dominant inheritance in the other. They also described postmortem studies of people with MMND, and found that the spinal cord had extreme loss of anterior horn cells and demyelination and sclerosis of the ventrolateral columns; which could explain peripheral weakness, paresthesias, or paralysis. They also found changes in the color of the myelin of the optic nerves, decreases in Purkinje cells, increase in Bergman glia, demyelination of fibers around the dentate nucleus with gliosis, swollen globular neurons of deep nuclei of the cerebellum, neural depletion and gliosis of the cochlear nucleus on both sides of the brainstem, and demyelination and axonal loss of the cochlear nerve.
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Overdose of sumatriptan can cause sulfhemoglobinemia, a rare condition in which the blood changes from red to green, due to the integration of sulfur into the hemoglobin molecule. If sumatriptan is discontinued, the condition reverses within a few weeks. Serious cardiac events, including some that have been fatal, have occurred following the use of sumatriptan injection or tablets. Events reported have included coronary artery vasospasm, transient myocardial ischemia, myocardial infarction, ventricular tachycardia, and ventricular fibrillation (V-Fib). The most common side effects reported by at least 2% of patients in controlled trials of sumatriptan (25-, 50-, and 100-mg tablets) for migraine are atypical sensations (paresthesias and warm/cold sensations) reported by 4% in the placebo group and 5–6% in the sumatriptan groups, pain and other pressure sensations (including chest pain) reported by 4% in the placebo group and 6–8% in the sumatriptan groups, neurological events (vertigo) reported by less than 1% in the placebo group and less than 1% to 2% in the sumatriptan groups.
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The oral form of the drug has boxed warnings concerning the risks of retinoic acid syndrome and leukocytosis. Other significant side effects include a risk of thrombosis, benign intracranial hypertension in children, high lipids (hypercholesterolemia and/or hypertriglyceridemia), and liver damage. There are many significant side effects from this drug that include malaise (66%), shivering (63%), hemorrhage (60%), infections (58%), peripheral edema (52%), pain (37%), chest discomfort (32%), edema (29%), disseminated intravascular coagulation (26%), weight increase (23%), injection site reactions (17%), anorexia (17%), weight decrease (17%), and myalgia (14%). Respiratory side effects usually signify retinoic acid syndrome, and include upper respiratory tract disorders (63%), dyspnea (60%), respiratory insufficiency (26%), pleural effusion (20%), pneumonia (14%), rales (14%), and expiratory wheezing (14%), and many others at less than 10%. Around 23% of people taking the drug have reported earache or a feeling of fullness in their ears. Gastrointestinal disorders include bleeding (34%), abdominal pain (31%), diarrhea (23%), constipation (17%), dyspepsia (14%), and swollen belly (11%) and many others at less than 10%. In the cardiovascular system, side effects include arrhythmias (23%), flushing (23%), hypotension (14%), hypertension (11%), phlebitis (11%), and cardiac failure (6%) and for 3% of patients: cardiac arrest, myocardial infarction, enlarged heart, heart murmur, ischemia, stroke, myocarditis, pericarditis, pulmonary hypertension, secondary cardiomyopathy. In the nervous system, side effects include dizziness (20%), paresthesias (17%), anxiety (17%), insomnia (14%), depression (14%), confusion (11%), and many others at less than 10% frequency.
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