Biomedical subjects
G McCarthy
Publications and source records attributed to G McCarthy.
Does interictal spiking change prior to seizures?
We studied 10 patients with intractable epilepsy being evaluated for epilepsy surgery for preictal changes in spiking. All patients were implanted with intracranial electrodes and underwent continuous EEG/audiovisual monitoring. Interictal spikes were detected and recorded continuously by a dedicated computerized system. Edited spikes were counted during 0-5, 5-10, and 0-60 min epochs before each seizure, during epochs of unvarying state of arousal (awake or sleep stage II). When comparing by repeated measures, 1-way ANOVA, total spiking (in all recording channels) did not differ among the different preictal epochs (0-5, 5-10, 0-60 min) in 45 seizures (F = 0.88, P = 0.40, using the Geisser-Greenhouse adjustment--GGA). Likewise, no significant differences were obtained during those same epochs when comparing spiking originating from the channel of seizure onset in 5 patients with 28 seizures of localized onset (F = 1.19, P = 0.38 using the GGA). Our findings indicate that in patients with intractable epilepsy, no changes in spiking occur in the 5 min prior to seizures, when compared to more distant preictal epochs.
Effect of H2-receptor antagonist pretreatment on vecuronium- and atracurium-induced neuromuscular block.
Seventy-two patients were studied in a double-blind randomized controlled design to assess the effects of oral administration of cimetidine 400 mg, ranitidine 150 mg or placebo 90 min before anaesthesia on the neuromuscular blocking effects of atracurium 0.45 mg kg-1 or vecuronium 0.08 mg kg-1. The times to reappearance of T1 (first response in the train-of-four stimulation) and its recovery to 25% of control were 22.5 (SD) 5.2 and 30 (7.1) min, 30 (10) and 43 (15.4) min, and 25.8 (4.1) and 34 (6.2) min, respectively in the vecuronium groups pretreated with placebo, cimetidine and ranitidine, the times following cimetidine pretreatment being prolonged significantly (P less than 0.05). The respective recovery indices (times for 25-75% recovery of T1) in these three groups were 11.0 (3.5), 17.4 (6.8) and 13.0 (3.9) min. There were no significant differences in any of the variables following ranitidine pretreatment and either neuromuscular blocker or following cimetidine pretreatment and atracurium.
Potentials evoked in human and monkey cerebral cortex by stimulation of the median nerve. A review of scalp and intracranial recordings.
Somatosensory evoked potentials (SEPs) are generated in afferent pathways, subcortical structures and various regions of cerebellar and cerebral cortex by stimulation of somatic receptors or electrical stimulation of peripheral nerves. This review summarizes current knowledge of SEPs generated in cerebral cortex by stimulation of the median nerve, the most common form of stimulation for human research and clinical investigations. Major sources of data for the review are intracranial recordings obtained from patients during diagnostic or neurosurgical procedures, and similar recordings in monkeys. Short-latency cortical SEPs in the 20-40 ms latency range consist of P20 and N30, recorded from motor cortex and frontal scalp; P25 and N35, recorded from cortex near the central sulcus and central scalp; and N20 and P30, recorded from somatosensory cortex and parietal scalp. Several lines of evidence including cortical surface and intracerebral recordings, neuromagnetic recordings and lesion studies in humans and monkeys, strongly support the conclusion that these potentials are generated in contralateral somatosensory cortex in areas 3b and 1, in contrast to the conclusion of many previous studies that SEPs recorded from the frontal scalp are generated in motor cortex and other frontal lobe areas. These potentials are primarily mediated by cutaneous afferents of the dorsal column-medial lemniscal system; the contribution of muscle afferents has not been completely resolved but appears to be small. There is currently no evidence that short-latency SEPs are generated in cortex other than primary somatosensory cortex. Recordings from the vicinity of the second somatosensory area, from the supplementary motor and sensory areas and from surface cortex other than sensorimotor cortex have not detected reliable short-latency activity, although some of these regions generate long-latency potentials. Consequently, short-latency SEPs recorded from the scalp are similar to those recorded from the surface of sensorimotor cortex. Old World monkeys such as Macaca mulatta and M. fascicularis provide an excellent model for human short-latency SEPs. All the potentials described above in humans have corresponding monkey analogues, with similar distributions over the cortical surface. The squirrel monkey, a New World species, exhibits the same potentials, but due to the different morphology of sensorimotor cortex, the surface distribution of SEPs is quite different.
Twenty-four-hour ambulatory blood pressure in men and women aged 17 to 80 years: the Allied Irish Bank Study.
In order to determine reference values for ambulatory blood pressure, a sample of 815 healthy bank employees (399 men and 416 women), aged 17-79 years, were investigated. Ambulatory blood pressure was recorded over 24 h, taking measurements at 30-min intervals. Blood pressure was also measured by trained observers in the clinic. Ambulatory blood pressure in the 815 subjects averaged 118/72 mmHg over 24 h, 124/78 mmHg during the day (1000-2259 h) and 106/61 mmHg at night (0100-0659 h). Office blood pressure, measured by an observer, was 4/2 mmHg lower (p less than 0.0001) than daytime ambulatory pressure. The 95th centiles for the daytime ambulatory pressure in men were: 114/88 mmHg for the age group 17-29 years (n = 107); 143/91 mmHg from 30-39 years (n = 123); 150/98 mmHg from 40-49 years (n = 109); and 155/103 mmHg in 50-79 year old men (n = 60); for the corresponding age groups in women, the 95th centiles of the daytime pressure were: 131/83 mmHg (n = 174); 132/85 mmHg (n = 149); 150/94 mmHg (n = 55); and 177/97 mmHg (n = 38).
A comparison of different pre-oxygenation techniques in the elderly.
The efficacy of five different techniques of pre-oxygenation before a modified rapid intubation sequence was assessed, using oxygen saturation measurement, in patients aged over 65 years. Twenty patients in each group were pre-oxygenated using four deep breaths or normal tidal breathing for 1, 2, 3, or 4 minutes. The acceptable period of apnoea was defined as the time taken to desaturate to 93%. The mean times (SD) taken to reach this end-point were 3.7 (1.6), 4.1 (1.2), 5.4 (1.7), 5.4 (1.4) and 5.2 (1.7) minutes respectively. The apnoea times with 2, 3 and 4 minutes pre-oxygenation were not significantly different from each other but were significantly longer than after four deep breaths and 1 minute. It is concluded that a pre-oxygenation period of at least 2 minutes should be employed in the elderly before a rapid sequence induction.
Cortical somatosensory evoked potentials. I. Recordings in the monkey Macaca fascicularis.
1. The anatomic generators of somatosensory evoked potentials (SEPs) to median nerve stimulation in the 10- to 30-ms latency range were investigated in monkeys (Macaca fascicularis) by means of cortical-surface and laminar recordings. 2. Three groups of SEPs evoked by stimulation of the contralateral median nerve were recorded from the hand representation area of sensorimotor cortex: P10-N20, recorded anterior to the central sulcus (CS); N10-P20, recorded posterior to the CS; and P12-N25, recorded near the CS. These potentials were similar in morphology and surface distribution whether the animal was awake or anesthetized. 3. P10-N20 exhibited a polarity inversion to N10-P20 across the CS, both in cortical-surface recordings and in laminar recordings within cortex and white matter of motor and somatosensory cortex. In contrast, P10-N20 and N10-P20 did not exhibit polarity inversion in recordings from the surface and white matter of the crowns of motor and somatosensory cortex, respectively. These results strongly suggest that these potentials are produced by a tangential generator located in the posterior wall of the CS, primarily in area 3b of somatosensory cortex. 4. P12-N25 was largest over the hand area of somatosensory cortex and showed polarity inversion across the crown of somatosensory cortex but not across the crown of motor cortex or across the walls of the CS, suggesting that P12-N25 is due to a radially oriented generator located in areas 1 and 2 of somatosensory cortex. 5. P10-N20 and P12-N25 are thought to be equivalent to the "primary evoked response" recorded from somatosensory cortex of other mammals. 6. These results are very similar to those obtained in human cortical-surface recordings and demonstrate that the monkey P10-N20, N10-P20, and P12-N25 potentials correspond to the human P20-N30, N20-P30, and P25-N35 potentials, respectively. The only appreciable difference in human and monkey SEPs is that the monkey P12-N25 appears to be generated in areas 1 and 2, whereas the human P25-N35 appears to be generated only in area 1. 7. There was no evidence of locally generated activity in areas 3a and 4.
Cortical somatosensory evoked potentials. II. Effects of excision of somatosensory or motor cortex in humans and monkeys.
1. To clarify the generators of human short-latency somatosensory evoked potentials (SEPs) thought to arise in sensorimotor cortex, we studied the effects on SEPs of surgical excision of somatosensory or motor cortex in humans and monkeys. 2. Normal median nerve SEPs (P20-N30, N20-P30, and P25-N35) were recorded from the cortical surface of a patient (G13) undergoing a cortical excision for relief of focal seizures. All SEPs were abolished both acutely and chronically after excision of the hand area of somatosensory cortex. Similarly, excision of the hand area of somatosensory cortex abolished corresponding SEPs (P10-N20, N10-P20, and P12-N25) in monkeys. Excision of the crown of monkey somatosensory cortex abolished P12-N25 while leaving P10-N20 and N10-P20 relatively unaffected. 3. After excision of the hand area of motor cortex, all SEPs were present when recorded from the cortical surface of a patient (W1) undergoing a cortical excision for relief of focal seizures. Similarly, all SEPs were present in monkeys after excision of the hand area of motor cortex. 4. Although all SEPs were present after excision of motor cortex in monkeys, variable changes were observed in SEPs after the excisions. However, these changes were not larger than the changes observed after excision of parietal cortex posterior to somatosensory cortex. We concluded that the changes were not specific to motor cortex excision. 5. These results support two major conclusions. 1) Median nerve SEPs recorded from sensorimotor cortex are produced by generators in two adjacent regions of somatosensory cortex: a tangentially oriented generator in area 3b, which produces P20-N30 (human) and P10-N20 (monkey) [recorded anterior to the central sulcus (CS)] and N20-P30 (human) and N10-P20 (monkey) posterior to the CS; and a radially oriented generator in area 1, which produces P25-N35 (human) and P12-N25 (monkey) recorded from the postcentral gyrus near the CS. 2) Motor cortex makes little or no contribution to these potentials.
Intraarticular corticosteroids possibly leading to local osteonecrosis and marrow fat induced synovitis.
We describe a woman with recurrent synovitis in one or both knees treated with intraarticular corticosteroid injections and two 6-day courses of methylprednisolone tablets. She later developed osteonecrosis of her distal femora and proximal tibiae. Her course was complicated by persistent synovitis associated with a large quantity of necrotic fat in the joint fluid.
Functional organization of human supplementary motor cortex studied by electrical stimulation.
The presence of somatotopic organization in the human supplementary motor area (SMA) remains a controversial issue. In this study, subdural electrode grids were placed on the medial surface of the cerebral hemispheres in 13 patients with intractable epilepsy undergoing evaluation for surgical treatment. Electrical stimulation mapping with currents below the threshold of afterdischarges showed somatotopic organization of supplementary motor cortex with the lower extremities represented posteriorly, head and face most anteriorly, and the upper extremities between these two regions. Electrical stimulation often elicited synergistic and complex movements involving more than one joint. In transitional areas between neighboring somatotopic representations, stimulation evoked combined movements involving the body parts represented in these adjacent regions. Anterior to the supplementary motor representation of the face, vocalization and speech arrest or slowing of speech were evoked. Various sensations were elicited by electrical stimulation of SMA. In some cases a preliminary sensation of "urge" to perform a movement or anticipation that a movement was about to occur were evoked. Most responses were contralateral to the stimulated hemisphere. Ipsilateral and bilateral responses were elicited almost exclusively from the right (nondominant) hemisphere. These data suggest the presence of combined somatotopic organization and left-right specialization in human supplementary motor cortex.
Perianal appearances associated with constipation.
The perianal appearances were studied prospectively of 136 constipated children (mean age 3.9 years, 67 boys, 69 girls). Anal dilatation, fissures, tags, warts, perianal oedema, redness, blueness, and veins were recorded. It was noted whether dilatation occurred immediately or at 30 and 60 seconds with the buttocks minimally separated, and on subsequent firm lateral traction of the buttocks. The degree of faecal loading was assessed in all children. Anal dilatation was found in 24 (18%) and first appeared on lateral traction in eight (6%). In three quarters of the children with dilatation faecal loading or perianal signs were present. Fissures were found in 35 (26%) children and tags in seven (5%). Perianal redness was more likely to be associated with fissures, and blueness with dilatation. We conclude that there are no pathognomonic perianal signs in childhood constipation and that the technique of anal examination should be standardised.
Mild hypoglycemia and impairment of brain stem and cortical evoked potentials in healthy subjects.
To evaluate the impact of mild hypoglycemia on CNS function in healthy adults, we measured brain stem auditory evoked potentials and P300 potentials (elicited by cognitive processing of auditory stimuli) during hypoglycemic or euglycemic insulin clamps (80 mU.m-2.min-1). In the hypoglycemic clamp study (n = 8), plasma glucose was allowed to fall from 4.6 to 3 mM in hourly approximately 0.5-mM steps and subsequently returned to euglycemic baseline levels. In the euglycemic clamp study (n = 8), plasma glucose was maintained at baseline levels throughout. Neither brain stem nor P300 responses changed during the euglycemic control study; symptoms and counterregulatory hormones were also unaffected. During the hypoglycemia study, epinephrine and growth hormone rose once plasma glucose reached 3.4 +/- 0.1 mM. Brain stem and P300 potentials remained unchanged until the 3-mM glucose step, when neurophysiological changes suddenly developed in conjunction with reported symptoms. At this glucose level, the wave V component of the brain stem potential was selectively altered in 7 of 8 subjects. Furthermore, P300 latency significantly increased, and amplitude diminished. Changes in both brain stem and cortical (P300) responses reversed when euglycemia was restored. We conclude that modest reductions in plasma glucose (to 3 mM) produce marked alterations in both brain stem and cortical responses to auditory stimuli. These changes in neural function appear at the same time as symptoms and follow rather than precede the rise in counterregulatory hormones during hypoglycemia. Our data suggest that the adverse effects of mild hypoglycemia on brain function are not limited to higher centers but also involve the brain stem.
Obstacles to the treatment of detainees in South Africa.
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Severe disability in rheumatoid arthritis: assessment following comprehensive rehabilitation.
26 patients with rheumatoid arthritis (RA) who presented with severe disability to a rheumatology unit were reviewed following comprehensive rehabilitation. This comprised in-patient evaluation, alteration in drug therapy, physical and occupational therapy and in many cases, orthopaedic surgery. Sustained benefit is observed 4-6 years later in terms of disease activity and functional class. The greatest improvement in functional class was noted in those patients who underwent joint replacement.
Reflex sympathetic dystrophy associated with large cell lung carcinoma.
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Human cortical potentials evoked by stimulation of the median nerve. I. Cytoarchitectonic areas generating short-latency activity.
1. The anatomic generators of human median nerve somatosensory evoked potentials (SEPs) in the 40 to 250-ms latency range were investigated in 54 patients by means of cortical-surface and transcortical recordings obtained during neurosurgery. 2. Contralateral stimulation evoked three groups of SEPs recorded from the hand representation area of sensorimotor cortex: P45-N80-P180, recorded anterior to the central sulcus (CS) and maximal on the precentral gyrus; N45-P80-N180, recorded posterior to the CS and maximal on the postcentral gyrus; and P50-N90-P190, recorded near and on either side of the CS. 3. P45-N80-P180 inverted in polarity to N45-P80-N180 across the CS but was similar in polarity from the cortical surface and white matter in transcortical recordings. These spatial distributions were similar to those of the short-latency P20-N30 and N20-P30 potentials described in the preceding paper, suggesting that these long-latency potentials are generated in area 3b of somatosensory cortex. 4. P50-N90-P190 was largest over the anterior one-half of somatosensory cortex and did not show polarity inversion across the CS. This spatial distribution was similar to that of the short-latency P25-N35 potentials described in the preceding paper and, together with our and Goldring et al. 1970; Stohr and Goldring 1969 transcortical recordings, suggest that these long-latency potentials are generated in area 1 of somatosensory cortex. 5. SEPs of apparently local origin were recorded from several regions of sensorimotor cortex to stimulation of the ipsilateral median nerve. Surface and transcortical recordings suggest that the ipsilateral potentials are generated not in area 3b, but rather in other regions of sensorimotor cortex perhaps including areas 4, 1, 2, and 7. This spatial distribution suggests that the ipsilateral potentials are generated by transcallosal input from the contralateral hemisphere. 6. Recordings from the periSylvian region were characterized by P100 and N100, recorded above and below the Sylvian sulcus (SS) respectively. This distribution suggests a tangential generator located in the upper wall of the SS in the second somatosensory area (SII). In addition, N125 and P200, recorded near and on either side of the SS, suggest a radial generator in a portion of SII located in surface cortex above the SS. 7. In comparison with the short-latency SEPs described in the preceding paper, the long-latency potentials were more variable and were more affected by intraoperative conditions.(ABSTRACT TRUNCATED AT 400 WORDS)
Human cortical potentials evoked by stimulation of the median nerve. II. Cytoarchitectonic areas generating long-latency activity.
1. The anatomic generators of human median nerve somatosensory evoked potentials (SEPs) in the 40 to 250-ms latency range were investigated in 54 patients by means of cortical-surface and transcortical recordings obtained during neurosurgery. 2. Contralateral stimulation evoked three groups of SEPs recorded from the hand representation area of sensorimotor cortex: P45-N80-P180, recorded anterior to the central sulcus (CS) and maximal on the precentral gyrus; N45-P80-N180, recorded posterior to the CS and maximal on the postcentral gyrus; and P50-N90-P190, recorded near and on either side of the CS. 3. P45-N80-P180 inverted in polarity to N45-P80-N180 across the CS but was similar in polarity from the cortical surface and white matter in transcortical recordings. These spatial distributions were similar to those of the short-latency P20-N30 and N20-P30 potentials described in the preceding paper, suggesting that these long-latency potentials are generated in area 3b of somatosensory cortex. 4. P50-N90-P190 was largest over the anterior one-half of somatosensory cortex and did not show polarity inversion across the CS. This spatial distribution was similar to that of the short-latency P25-N35 potentials described in the preceding paper and, together with our and Goldring et al. 1970; Stohr and Goldring 1969 transcortical recordings, suggest that these long-latency potentials are generated in area 1 of somatosensory cortex. 5. SEPs of apparently local origin were recorded from several regions of sensorimotor cortex to stimulation of the ipsilateral median nerve. Surface and transcortical recordings suggest that the ipsilateral potentials are generated not in area 3b, but rather in other regions of sensorimotor cortex perhaps including areas 4, 1, 2, and 7. This spatial distribution suggests that the ipsilateral potentials are generated by transcallosal input from the contralateral hemisphere. 6. Recordings from the periSylvian region were characterized by P100 and N100, recorded above and below the Sylvian sulcus (SS) respectively. This distribution suggests a tangential generator located in the upper wall of the SS in the second somatosensory area (SII). In addition, N125 and P200, recorded near and on either side of the SS, suggest a radial generator in a portion of SII located in surface cortex above the SS. 7. In comparison with the short-latency SEPs described in the preceding paper, the long-latency potentials were more variable and were more affected by intraoperative conditions.
Task-dependent field potentials in human hippocampal formation.
Task-dependent field potentials were recorded from implanted electrodes located in the hippocampus and other medial temporal lobe (MTL) structures of epileptic patients undergoing evaluation for possible surgery. In 2-alternative categorization tasks, low-probability auditory, somatic, and visual stimuli elicited potentials with large amplitudes and sharp spatial gradients having the following characteristic spatial distribution: positive posterior to the hippocampus, negative within the hippocampus, and positive anterior to the hippocampus. The sharp spatial gradients within the MTL suggest that these potentials were locally generated, probably by hippocampal pyramidal cells. The MTL potentials were also reliably elicited by exemplars of semantic categories and by stimulus omissions and were sensitive to the sequence of preceding stimuli. However, they were not elicited by the same stimulus sequences when the patient's attention was directed elsewhere and categorization was not required. These results indicate that the MTL potentials reflect endogenous as opposed to obligatory processes. The time course and task dependence of the MTL potentials suggest that MTL structures could contribute to P300 and related event-related potentials on the scalp.