Disease relevance of Paresthesia

• Acute fluoride poisoning produces a clinical syndrome characterized by nausea, vomiting, diarrhea, abdominal pain, and paresthesias [1].
• Edema of the extremities, frequently accompanied by pruritus, paresthesia, and myalgia, developed in the nine patients (six women and three men; age range, 30 to 66 years) 1 to 18 months after the start of therapy with tryptophan (1.5 to 3.0 g daily) for insomnia, depression, or obesity [2].
• The selective response of demyelinated sensory fibers to 4-aminopyridine (4-AP) has been proposed as a mechanism underlying the reported paresthesias that complicate the use of this potassium-channel blocking agent in clinical trials for the treatment of multiple sclerosis and neuromuscular disorders [3].
• However, subjective side effects such as paresthesias, dizziness, and light-headedness were frequently reported during 4-aminopyridine treatment [4].
• Side-effects during acetazolamide therapy included paresthesias in 5 patients and renal calculus in 1 [5].

Psychiatry related information on Paresthesia

• BACKGROUND: GSS, associated with a missense mutation at codon 102 of the prion protein (PrP) gene (GSS102), is a hereditary disorder that presents with progressive ataxia and dementia, and is characterized by the loss of deep tendon reflexes and painful dysesthesias of the legs in its early stage [6].
• Step-by-step adjustment of pulse output parameters was performed at the electrode configuration at which paresthesias occurred ("sensory threshold"), covered the anginal area ("adjusted setting"), or provoked pain ("motor threshold") [7].

High impact information on Paresthesia

• Adverse events included nausea, circumoral paresthesia, elevated hepatic aminotransferase levels, and elevated triglyceride levels [8].
• Astemizole-induced paresthesia [9].
• Several traditional findings of CTS have little or no diagnostic value, including nocturnal paresthesias; Phalen and Tinel signs; thenar atrophy; and 2-point, vibratory, and monofilament sensory testing [10].
• Adverse events significantly associated with tacrolimus, including headache, increased serum creatinine level, insomnia, leg cramps, paresthesias, and tremor, were managed with dose reduction [11].
• Paresthesias and mefloquine prophylaxis [12].

Chemical compound and disease context of Paresthesia

• Peripheral nerve symptoms consisting of paresthesias, motor weakness, or sensory impairment have been associated with the use of the penicillins, sulfonamides, chloramphenicol, colistin, metronidazole, isoniazid, ethionamide, and dapsone [13].
• Formication and azathioprine therapy [14].
• Some patients had features not usually associated with botulism including paresthesia (14%), asymmetric extremely weakness (17%), asymmetric ptosis (8%), slightly elevated cerebrospinal fluid protein values (14%), and positive responses to edrophonium chloride(26%) [15].
• A significantly greater incidence of drug-related nausea, vomiting, rash and oral/perioral paresthesia was observed with amprenavir/lamivudine/zidovudine than with lamivudine/zidovudine [16].
• No significant changes were observed in symptoms of pain, numbness, or paresthesia between ponalrestat and placebo groups, and there were no improvements in VPT or TT at several sites [17].

Biological context of Paresthesia

• Occupational exposure to pyrethroids frequently leads to paresthesia and respiratory irritation, which are probably due to repetitive firing of sensory nerve endings [18].
• The most frequently reported adverse events after CI-977 administration were dizziness, fatigue, paresthesia, headache, vasodilatation (facial flushing), emotional lability, high feeling, and abnormal thinking [19].
• Not only were subjective complaints of tremor, palpitations, and paresthesias increased for metaproterenol, but the heart rate response was significantly elevated (p less than 0.05) compared with glycopyrrolate [20].
• A 32-year-old fumigation assistant developed systemic and neuro-ophthalmic manifestations of methyl bromide poisoning, including increased serum bromide level (6.6 mg/100 ml), paresthesias and burning dysesthesia on his hands and feet, and visual impairment [21].
• Disadvantages with fosphenytoin include rate and dose related paresthesias and pruritis, delayed decreases in blood pressure, the potential for therapeutic drug monitoring errors, and higher drug acquisition costs [22].

Anatomical context of Paresthesia

• Eleven patients (5%) had apparent tonic-clonic seizure-like activity, and 7 patients (3%) had non-tonic-clonic neurologic events, including focal seizures (n = 3), dysarthria or aphasia (n = 2), unilateral extremity dysesthesia (n = 1), and reproduction of temporal lobe epilepsy symptoms (n = 1) [23].
• CONCLUSIONS: The PrP abnormalities in synaptic structures of the spinal posterior horn may cause synaptic dysfunction that leads to loss of deep tendon reflexes and painful dysesthesias in patients with GSS102 [6].
• Chronic application of alumina cream to the trigeminal ganglion in 10 cats failed to produce a long-lasting behavioral syndrome of facial dysesthesia [24].
• The present data provide clinical evidence that the development of central dysesthesia pain after traumatic spinal cord injury is dependent on the activation of central NMDA receptors [25].
• Subjects suffering from traumatic dysesthesia of the trigeminal nerve were treated with capsaicin, a substance P depleter with significant long-term effects [26].

Gene context of Paresthesia

• Paresthesias, often described as electric shocks (Lhermitte sign), were common in GDNF-treated subjects, were not dose related, and resolved on discontinuation of GDNF [27].
• After IFN-beta treatment, HCV RNA was cleared from serum without severe adverse effects, including paresthesias [28].
• Because severe paresthesias occurred with initial daily administration of 5 million units (MU) of lymphoblastoid IFN-alpha, the dose was reduced to 3 to 6 MU of IFN-alpha2b three times a week [28].
• PRTG was associated wtih an 8% risk of complications, which included anesthesia dolorosa, corneal anesthesia with keratitis, and significant facial paresthesias [29].
• In group S (single injection, n = 53) 80 mL MEPE 1% were injected into the neurovascular sheath, transarterially or after eliciting paresthesia [30].

Analytical, diagnostic and therapeutic context of Paresthesia

• Independent risk factors for paresthesia/dysesthesia were postoperative monitoring in intensive care, age less than 40 yr, and use of bupivacaine [31].
• Sublingual administration of Piroxicam FDDF was well tolerated: no systemic side-effects were reported and only two subjects complained about mouth dysesthesias which were described as mild and short-lasting [32].
• No side effects were observed during apheresis procedures except for transient paresthesia episodes promptly resolved with the administration of calcium gluconate [33].
• In three of these patients, the system was ineffective after a period of 3-9 months despite paresthesia in the area of anginal pain with electrical stimulation [34].
• BACKGROUND AND OBJECTIVES: Transient radiating back and leg pain defined as pain or dysesthesias in the buttocks, thighs, or calves within 24 to 48 hours after recovery from spinal anesthesia has been described with the use of 2% and 5% lidocaine [35].

References