Cortical Sign Research Articles

Scapho-lunate distance and cortical ring sign

The scapho-lunate distance was measured on posteroanterior radiographs of 100 normal wrists. The scapho-lunate distance measured a mean of 3.7 mm ± SD 0.6 (range from 2.5 to 5.0 mm). The mean for 44 male wrists was 4.0 mm, and for 56 female wrists it was 3.6 mm. These results indicate that a scapho-lunate distance of up to 5 mm is not necessarily indicative of carpal instability. None of these normal wrists had a scaphoid “cortical ring” sign.

Cerebral potentials and electromyographic responses evoked by stretch of wrist muscles in man.

The cerebral evoked potential produced by rapid extension of the wrist was recorded from scalp electrodes in normal subjects while they exerted a small background flexor torque (0.24 Nm) against an electric motor. The initial part of the response consisted of a negative deflection (N1) with an average latency of 24.7 ms. This was followed by a biphasic P1/P2 (32 ms) response and a large later negative wave (N2) (76 ms). Passive wrist extension also evoked reflex EMG responses in the forearm flexor muscles which could be resolved into a short latency (25 ms) and long-latency (52 ms) component. The cerebral responses persisted almost unchanged during complete ischaemic anaesthesia of the hand produced by a pressure cuff around the wrist, and were reduced if the stretch was given during voluntary wrist flexion. The primary component (N1-P1/P2) of the cerebral response probably represents the arrival at the cortex of the muscle afferent volley. However, the significance of the secondary component (P1/P2-N2) is unknown. Under certain conditions, its size was related to the size of the long latency stretch reflex evoked by stretch of the flexor muscles. Thus, increasing the velocity of stretch or decreasing the repetition rate (from 1.0 to 0.15 Hz) at which stretches were applied, increased the size of both the muscle reflex and the cerebral response. The secondary component also could be changed by voluntary reaction to wrist stretch. Changes in the size of the secondary component of the evoked response may represent the earliest cortical sign of interaction between sensory input and motor output.

Computed tomography differentiation of pyelonephritis and renal infarction

Acute renal infarction and acute pyelonephritis can have identical clinical presentations. Most of the computed tomography findings seen in acute renal infarction are similar to those in acute pyelonephritis, except for the characteristic cortical rim sign seen in acute infarction. This finding differentiates these two disorders. This sign may be subtle and not appreciated unless searched for diligently with appropriate computed tomography imaging at varying window settings with particular attention to the subcapsular region.

Event related brain potentials and human pain: A first objective overview

Since 1960 systematic studies of the human scalp-conducted cerebral slow-wave response to painful stimulation have shown only amplitude augmentation of the vertex components of the somatosensory evoked potential (SEP) to be indicators of subjective perception of a noxious or aversive quality in the stimulus. The vertex potential (VP) of the SEP occurs relatively late after onset of either transient or maintained stimuli (100–400 ms depending on stimulus mode and site), is amplitude-focal at vertex on scalp, and may be asymmetrically distributed hemispherically for unilateral stimulation of the hands. Its functional neuroanatomy seems undeterminable by scalp macroelectrodes, and its relationship to analogous vertex potentials in the auditory and visual modalities (AEP and VEP) unknown. Studies of the nociceptive SEP (SEPn) since 1977 concur that VP amplitude is more readily correlatable with subjective pain magnitude estimate than with objective stimulus parameters. They also suggest that the VP is amplitude-sensitive to (a) interstimulus-intervals less than about 350 ms; (b) analgesics and their antagonists; and (c) subjective cognitive status with regard to both the expected aversiveness of the stimulus and the previous experience of chronic pain. These studies have included electrical stimulation of toothpulp and teeth, mechanical and transcutaneous electrical stimulation of palmar and digital glabrous skin, noxious thermal stimulation of hands and forearms, and electrical stimulation of lips, fingers, toes, and anogenital perineum of both sexes. They have been done in the context of both classical and signal-detectability (TSD) methods for concurrent reports of painful versus painless, and in the methodological contexts of conventionally signal-averaged SEP and of single-epoch SEP recovered both raw and processed. Studies designed to analyze differences in the early-intermediate (25–95 ms) and late (500–1000 ms) time-segments of SEP for painful and painless stimulation have provided no convincing evidence of cortical nociceptive signals. Therefore existing data on the SEPn imply that the only cortical slow-wave sign of nociception reflects perceptual-cognitive and endogenous, rather than sensory-discriminative and exogenous, aspects of the conscious pain experience.

Renal infarction: CT diagnosis and correlation between CT findings and etiologies.

The CT scans and the clinical records of 12 patients who had renal infarction were reviewed. The renal infarcts were classified as either focal or global. The CT findings were correlated with the etiologies of renal infarction. Embolism was the most common cause of renal infarcts that were multifocal with involvement of both kidneys. Trauma caused a unilateral global type of infarct. A case of sickle cell anemia presented with multiple "slit-like" focal infarcts and enlarged kidneys. Forty-seven per cent of infarcts demonstrated the cortical rim sign, 11% were associated with mass effect, 21% had a subcapsular fluid collection, and 6% had an abnormally thickened renal fascia.

The cognitive P40, N60 and P100 components of somatosensory evoked potentials and the earliest electrical signs of sensory processing in man

Selective attention tasks involving random sequences of electrical stimulation of fingers were designed to compare cerebral potentials to identical stimuli (for example to the left thumb) when they are ‘infrequent target’ signals or ‘frequent-neglected’ signals in the series. The experiments were carried out in normal adult subjects. The early SEP components were analyzed for the earliest cortical electrical sign of information processing stages. Two new components, P40 (with onset at 26 msec) and N60, precede the processing positivity P100 which may be more significant in somatosensory processing than the negativities recorded in auditory or visual tasks.

Radiological evaluation of cortical rim sign of the kidney

Radiological evaluation of cortical rim sign of the kidney

Renal Subcapsular Rim Sign: New Etiologies and Pathogenesis

Two prior reports have described a cortical rim sign associated with renal infarction from acute renal artery obstruction. This paper adds four additional cases of a thin outer (subcapsular) cortical nephrogram due to renal vein thrombosis (two cases), acute tubular necrosis (one case), and renal artery embolization (one case). An acute vascular compromise from differing etiologic mechanisms appears to be the common denominator of the rim nephrogram. The nephrogram probably represents an intact subcapsular renal cortex (2-4 mm thick) perfused by the perirenal capsular collateral circulation. To date, the rim nephrogram has been visible only on high dose nephrotomography. Its smooth inner margin is sufficiently distinct to differentiate it from the shell nephrogram of severe hydronephrosis.

The cortical rim sign of renal infarction.

Abstract A case is described of bilateral renal infarction following graft replacement of an abdominal aortic aneurysm. The patient developed oliguric renal failure following operation. An intravenous urogram on the 27th post-operative day showed a thin dense rim around each kidney during the nephographic phase. This corresponded to a viable rim of cortex at post-mortem. It is likely that this was due to collateral circulation from the renal capsule. It is considered that this “nephrographic rim” sign is diagnostic of total renal infarction or cortical necrosis. Its demonstration depends on high-dose nephrotomography.