G Zuniga

Massachusetts General Hospital, Boston, MA, United States

Are you G Zuniga?

Claim your profile

Publications (7)44.07 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: We quantitated the size and configuration of compound muscle action potentials (CMAPs) in 266 nerves (66 median, 67 ulnar, 71 tibial and 62 peroneal) of 72 patients with acute inflammatory demyelinating polyneuropathy (AIDP) initially studied within 19 days of symptom onset. Results were compared with criteria for CMAP abnormalities, including criteria for abnormal negative peak duration and desynchronisation, derived from a control population of 50 median, ulnar, tibial and peroneal nerves. Other motor conduction abnormalities including minimal F response latency were also examined. We also analysed patterns of CMAP abnormality, peak disability and outcome for AIDP patients who had at least 3 motor nerves evaluated at first electrophysiologic study. Amongst AIDP nerves, low amplitude of the distal CMAP, usually with prolonged distal latency, was much more common than an abnormal fall in CMAP amplitude between stimulus sites. Using our CMAP criteria more than half of these low amplitude distal responses showed prolonged negative peak duration of desynchronisation or both, consistent with demyelination. Of the 47 AIDP patients who had 3 or more nerves initially studied, 37 (78.7%) had at least 1 motor nerve with a distal CMAP showing evidence of temporal dispersion. In addition, those with at least 75% of motor nerves showing a pattern of low amplitude of the distal CMAP without a further significant fall in amplitude between stimulus sites had greater peak disability and a poorer outcome. Assessment of temporal dispersion of the distal CMAP should be included in electrophysiologic criteria for acute demyelination. In addition, for some patients with AIDP patterns of CMAP amplitude abnormality amongst motor nerves are present early in the illness and may provide prognostic information.
    Electroencephalography and Clinical Neurophysiology 09/1994; 93(4):245-54. DOI:10.1016/0168-5597(94)90026-4
  • L Kiers, P Clouston, G Zuniga, D Cros
    [Show abstract] [Hide abstract]
    ABSTRACT: We examined F wave mean and minimum latency, mean and maximum amplitude, duration, persistence and chronodispersion in 241 nerves from 78 patients with Guillain-Barré syndrome (GBS) and 162 nerves from 43 patients with chronic inflammatory demyelinating polyneuropathy (CIDP). Results were compared with normal criteria derived from 72 median, 73 ulnar and 73 tibial control nerves, to determine the relative diagnostic sensitivity of the various F wave parameters. F wave abnormalities were found in 92% and 95% of nerves of patients with GBS and CIDP respectively. Absence of F responses or prolongation of minimum and mean latency were the most frequent abnormalities in both groups. Forty-five (11.2%) nerves overall had absent F responses with normal compound muscle action potential (CMAP) amplitudes and no significant fall between stimulus sites, consistent with isolated proximal conduction block. Forty-four nerves (23.7% of nerves in which F waves were present) fulfilled minimum F latency criteria for acquired demyelination . Eighty-one (20.1%) nerves had normal conventional motor nerve conduction studies and abnormal F responses, not all of which were identified by assessing only F absence or minimum latency. Severity of F wave abnormalities did not correlate with clinical outcome. Our findings confirm the high frequency of proximal nerve lesions in early GBS and CIDP, not all of which are associated with distal motor conduction abnormalities, and suggest that assessment of multiple F wave parameters, in particular chronodispersion, mean latency and mean amplitude (in addition to absence and minimum latency), increases the yield of F wave studies.
    Electroencephalography and Clinical Neurophysiology 09/1994; 93(4):255-64. DOI:10.1016/0168-5597(94)90027-2
  • J I Frank, A H Ropper, G Zuñiga
    [Show abstract] [Hide abstract]
    ABSTRACT: We studied the effects of acute intracranial lesions on the respiratory sinus arrhythmia (RSA) with the use of computerized measurements of the ratio of expiratory to inspiratory R-R intervals. The RSA was reduced below the 95th percentile for age in 20 of 27 patients, an average of 2 days after an acute event. Only four patients, without neurological deficits, had a normal RSA. Two patients, with signs of secondary brain-stem compression from a mass, had an increased RSA, without the bradycardia that is usually associated with Cushing's response. Twenty-three patients had their respiratory rate controlled by positive pressure ventilation during testing, and our preliminary findings suggested that this was not responsible for reducing the RSA. Acute intracranial lesions caused a diminished RSA, perhaps by reducing supratentorial influences on vagal cardioinhibitory activity. In contrast, once signs of secondary brain-stem compression occur, the RSA is greatly increased while the heart rate remains unchanged, offering a possible method of noninvasive monitoring for this complication.
    JAMA Neurology 12/1992; 49(11):1200-3. DOI:10.1001/archneur.1992.00530350122028
  • [Show abstract] [Hide abstract]
    ABSTRACT: We studied 34 patients with the Guillain-Barré syndrome (GBS) to clarify the clinical significance of inexcitable motor nerves and of low amplitude compound muscle action potentials (CMAPs). The patients were subdivided into two groups. Group 1 included eight patients who had electrically inexcitable motor nerves within 2 wks of the first symptom. (Two patients without extensive conduction studies had only one inexcitable motor nerve.) The outcome in this group at 1 yr varied from complete recovery (five patients) to severe motor sequelae (three patients). Group 2 included 26 patients who had two electrophysiological assessments, and in whom the serial changes in CMAP amplitudes were analysed and correlated to outcome. Fourteen of these 26 sets of serial studies were performed within 1 mth. Twelve of 26 patients in Group 2 showed decrease in the amplitude of CMAPs between serial studies; only six of these had a good outcome at 1 yr. Nine of 26 patients showed increase in CMAP amplitude between serial studies, of these eight had a good clinical outcome. Low-amplitude CMAPs or inexcitable motor nerves in the initial stages of GBS are due to distal pathology of the motor axons, either distal conduction block or axonal degeneration. The nature of these changes cannot be predicted by the results of the initial electrophysiological evaluation, including the presence or absence of active denervation. However, improvement of CMAP amplitude on sequential studies suggests a good outcome at 1 yr. We believe that, in the absence of a biological marker for GBS, individualization of an 'axonal variant' of the syndrome is not warranted at the present time.
    Brain 11/1992; 115 ( Pt 5):1291-302.
  • J I Frank, A H Ropper, G Zuniga
    [Show abstract] [Hide abstract]
    ABSTRACT: We present the hemodynamic and autonomic features of recurrent purely vasodepressor syncope episodes in a patient with left-sided malignant cervical adenopathy involving the carotid sinus. Extreme hypotension lasting 10 to 30 minutes, without change in heart rate, occurred spontaneously and 20 seconds after head-turning. The baseline respiratory sinus arrhythmia, heart rate response to standing and Valsalva's maneuver, and cold-induced blood pressure elevation were normal, indicating normal baroreceptor function between episodes. The episodes abated after 1 week of bedrest but reappeared within 1 day of discharge from the hospital. Syncope no longer occurred after intracranial section of the left glossopharyngeal nerve and upper rootlets of the left vagus. Autonomic testing remained normal postoperatively. A review of the literature indicates that purely vasodepressor syncope has been more common with left carotid sinus lesions.
    Neurology 07/1992; 42(6):1194-7. DOI:10.1212/WNL.42.6.1194
  • Brain 01/1992; 115(5):1291-1302. DOI:10.1093/brain/115.5.1291
  • G Zuniga, A H Ropper, J Frank
    [Show abstract] [Hide abstract]
    ABSTRACT: We studied 10 patients with sarcoidosis and peripheral neuropathy. Six had a subacute or chronic axonal sensorimotor neuropathy without cranial neuropathy, beginning months to years after established systemic sarcoidosis. One patient had severe enough diaphragmatic weakness to require mechanical ventilation. Four patients had atypical neuropathies: acute Guillain-Barré syndrome, mononeuritis multiplex, unilateral lumbosacral plexopathy, and a purely sensory neuropathy, all before systemic sarcoidosis became evident, and all except one had cranial nerve abnormalities. Autopsy in one patient with sensorimotor neuropathy showed only scattered foci of lymphocytes in spinal roots and ganglia with nerve fiber loss.
    Neurology 11/1991; 41(10):1558-61. DOI:10.1212/WNL.41.10.1558

Publication Stats

165 Citations
44.07 Total Impact Points


  • 1992
    • Massachusetts General Hospital
      • Surgical Intensive Care Unit
      Boston, MA, United States
  • 1991–1992
    • St. Elizabeth's Medical Center
      Boston, Massachusetts, United States