Median Nerve Neuropathy Research Articles

Motor potentials evoked by paired cortical stimuli

We recorded the motor evoked potentials (MEPs) from the abductor pollicis brevis muscle, after supramaximal electrical transcranial stimulation, and studied the effect of paired transcranial shocks with varying interstimulus time intervals, in 10 normal subjects, 4 patients with median nerve neuropathy and 2 patients with motoneurone disease. In relaxed muscles the amplitude of the MEP evoked by a single shock averaged 30% of the M wave. With intervals from 1 to 2.5 msec 2 shocks evoked one MEP far larger in size than the control MEP (70% of the M wave). With intervals of 10 msec and longer, the 2 shocks evoked 2 independent MEPs; the size of the MEP following the second shock (test) was inversely correlated with the size of the control MEP: the more the control MEP approached the size of the M wave, the smaller the test MEP. Single motor unit records showed that, in the normal subjects and patients with peripheral neuropathy, the same motor unit was activated either by the first or the second shock, whereas in the patients with motoneurone disease it fired twice. In active muscles, the control MEP averaged 70% of the M wave. With intervals of 10 msec and longer the test MEP was markedly suppressed; with 100 msec intervals it fully recovered. In relaxed muscles, by delivering a double shock at a 1.5 msec interval, thus evoking a large MEP, followed by a second double-shock, the test MEP was completely suppressed for a period of 20 msec; it began to recover at 50 msec intervals and fully recovered after 150 msec. These results indicate that: (1) high-threshold spinal motoneurones can profit from temporal summation if double-shocks are delivered at short time intervals; (2) the synchronous excitation of the motoneuronal pool produced by transcranial stimulation is followed by a 20 msec period of absolute inhibition, possibly through a massive activation of the Renshaw system; (3) during voluntary contraction, only a portion of the motoneuronal pool remains refractory, possibly because of the enhanced spinal excitability.

Saint anthony's fire or carpal tunnel syndrome?: A case of Iatrogenic Ergotism

A case of unilateral upper limb ischaemia from ergot overdosage is presented. An unusual feature was a median nerve neuropathy suggestive of carpal tunnel syndrome. The arteriographic appearances are demonstrated and management discussed.

Mediastinal pancreatic pseudocyst in infancy

1. Bucci G, Scalamandre A, Savignoni PG, Orzalesi M, and Mendicine M: Crib-side sampling of blood from the radial artery, Pediatrics 37:497, 1966. 2. Adams JM, Rudolph AJ: The use of indwelling radial artery catheters in neonates, Pediatrics 55:261, 1975. 3. Matthews JI, and Gibbons RB: Embolization complicating radial artery punctures, Ann Jntern Med 75:87, 1971. 4. Bedford RF, and Wollman H: Complications of percutaneous radial artery cannulation, Anesthesiology 38:228, 1973. 5. Mathieu A, Dalton B, Fischer JE, and Kumar A: Expanding aneurysm of the radial artery after frequent puncture, Anesthesiology 38:401, 1973. 6. Taylor N: Carpal tunnel syndrome, Am J Phy Med 50:192, 1971. 7. Koenigsberger MR, Curtin J, and Lovelace RE: Motor conduction velocities as a measure of gestational age in premature infants: a study of multiple births, twins, triplets, and quadruplets, Neurology 20:381, 1970. 8. Koenigsberger MR, Driscoll JM Jr, and Curtin J: Peripheral neuropathy in infants receiving intravenous hyperalimentation, proceedings of the Child Neurology Society, Hamilton, Ontario, Canada, October, 1975. 9. Thomas JE, and Lambert EH: Ulnar nerve conduction velocity and H-reflex in infants and children, J Appl Physiol 15:1, 1960. 10. Wagner AL, and Buchtal F: Motor and sensory conduction in infancy and childhood reappraisal, Dev Med Child Neurol 14:189, 1972. 11. Schulte FJ, Michaelis R, Linke I, and Nolte R: Motor nerve conduction velocity in term, preterm and small for dates newborn infants, Pediatrics 42:17, 1968. 12. Wigger HJ, Bransilver BR, and Blanc WA: Thrombosis due to catheterization in infants and children, J PEDIATR 76:1, 1970. 13. Nabseth D, and Jones JE: Gangrene of the lower extremities of infants after femoral venipuncture, N Engl J Med 268:1003, ~ 1963. 14. Macon WL, and Futrell JW: Median-nerve neuropathy after percutaneons puncture of the brachial artery in patients receiving anticoagulants, N Engl J Med 288:1396, 1973. 15. Starreveld E, and Ashenhurst EM: Bilateral carpal tunnel syndrome in childhood, Neurology 25:234, 1975. 16. Patten BM: Neuropathy induced by hemorrhage, Arch Neurol 21:381, 1969.

COMPRESSION NEUROPATHY FOLLOWING BRACHIAL ARTERIAL PUNCTURE IN ANTICOAGULATED PATIENTS

1) Seven patients were seen and treated over a 1-year span with forearm hematoma and median nerve neuropathy following brachial artery puncture. All seven were anticoagulated. 2) A careful examination established the diagnosis. Prompt operative intervention is recommended. 3) The brachial artery should be avoided as a source for arterial blood gas sampling in the anticoagulated patient.

NEUROPATHY, M COMPONENTS, AND AMYLOID

Of eighty-seven patients with non-hereditary systemic amyloidosis, ten had evidence of peripheral neuropathy. There was median-nerve neuropathy due to infiltration of the flexor retinaculum with amyloid in six patients. Two patients had diffuse sensorimotor neuropathy and two patients had sensory loss without evidence of motor impairment—three of these cases had amyloid deposition demonstrated by nerve biopsy. Neurological manifestations in all ten patients preceded other evidence of amyloidosis by 6 months-4 years (mean, 1·5 years). Neuropathy occurred in six of thirty-eight patients with primary amyloidosis and four of fourteen with amyloidosis associated with malignant B-cell dyscrasias; and all patients with neuropathy had either a serum-M-component or Bence-Jones proteinuria. In contrast, neuropathy was not noted in any of the fifty-six patients in this series who had no evidence of a monoclonal gammopathy (thirty-five with secondary and twenty-one with primary amyloidosis).

Median-nerve neuropathy after percutaneous puncture of the brachial artery in patients receiving anticoagulants.

SUBFASCIAL bleeding after percutaneous puncture of the brachial artery in patients on anticoagulation therapy may lead to median-nerve neuropathy and Volkmann's contracture, if not recognized and treated promptly.Case 1. A 17-year-old girl was given heparin because of consumptive coagulopathy. Blood for blood gas determination was obtained from the right brachial artery. Within a few hours swelling and discoloration were noted in the right elbow and forearm region. The radial pulse was absent although the capillary return was normal. The patient was treated with reversal of anticoagulation and arm elevation. The radial pulse returned in 2 days. After recovery from . . .

Median nerve neuropathy at the wrist.

Median nerve neuropathy at the wrist.

Diabetic hand syndrome

In this study two findings in diabetic neuropathy of the upper extremities are emphasized: flexion contractures of the fingers that may or may not be of the Dupuytren type, and delays in the transmission of median nerve motor impulses from the wrist to the hand of the degree usually considered to be diagnostic of a carpal tunnel syndrome. Such flexion contractures of the fingers correlate positively with the interval since the diagnosis of diabetes and are associated with slower transmission of motor nerve impulses in the forearm, variable delays in transmission of median and ulnar motor impulses from the wrist to the fingers, and decreased vibration perception. Delays in transmission of median nerve motor impulses from the wrist to the fingers of diabetic patients are accompanied about one-half of the time by similar delays in transmission of ulnar nerve motor impulses in the same hand. This suggests that findings in the median nerve suggestive of entrapment in the carpal tunnel are attributable at least in part, and perhaps entirely, to intrinsic median nerve neuropathy or myoneural dysfunction.