Are there false-negative results of motor evoked potential monitoring in brain surgery?

OBJECT: The present study explores the causes of occasional postoperative pareses despite unchanged or fully recovered intraoperative motor evoked potentials (MEPs) in supratentorial brain surgeries. METHODS: In a prospective, observational design, MEP monitoring results, motor outcome, and perioperative imaging were correlated in 200 procedures for brain tumours and cortical dysplasias critically related to motor areas and pathways. RESULTS: Persisting pareses after unchanged or recovered MEPs occurred in four cases due to delayed ischemia, or venous congestive oedema. Transient new deficit in four cases after stable MEP monitoring occurred due to inadvertently strong stimulation bypassing the target lesion, due to marked postresectional oedema, and after cortical transsections for alleviation of epilepsy. DISCUSSION AND CONCLUSIONS: With technically adequate MEP monitoring, truly false-negative results missing manifest corticospinal impairment do not occur. However, sustained vascular dynamics (vasospasm, congestive oedema) may cause delayed pareses which are missed, or hardly reflected by intraoperative MEP changes. Even minor MEP changes must therefore be observed to prevent impending motor deficit.

Intraoperative preservation of corticospinal function in the brainstem.

BACKGROUND: The corticospinal tract features a largely exposed course through the brainstem, and is therefore at risk in many brainstem-related procedures. No large case series on motor-evoked potential (MEP) monitoring during brainstem surgery have been reported as yet. OBJECTIVE: To understand intraoperative MEP changes during brainstem-related surgery, and to explore the value of MEP monitoring for preventing permanent new paresis. METHODS: Myogenic MEPs after transcranial electrical train stimulation were monitored in 70 cases of intraparenchymal (n = 39) and extraparenchymal (n = 31) brainstem-related tumours and vascular lesions. MEP recordings failed in another five cases. Motor outcome and intraoperative MEP results were documented prospectively and correlated for this study. RESULTS: Significant MEP changes occurred in 46% of cases. Stable and only reversibly deteriorated MEPs warranted unimpaired motor outcome (n = 50, 71% of all cases). Irreversible deterioration and reversible loss (n = 19, 27%) indicated a 37% risk for transient deficit. Irreversible loss (one case, 1.5%) predicted permanent paresis. MEPs and motor outcome correlated equally well in intra- and extraparenchymal lesions. Somatosensory-evoked potentials (SEPs) did not reliably reflect motor outcome. Permanent motor deficit occurred in one out five cases (20%) with failed MEP recordings. CONCLUSIONS: MEP monitoring-as opposed to SEPs-is a valid indicator of corticospinal function in brainstem-related surgery, independent from the type of lesion operated on. New deficit occurs only after more pronounced MEP changes than in supratentorial surgery, but complete loss as in spinal surgery is not required. MEPs may help to prevent permanent new paresis.

Stroke prevention during surgery for deep-seated gliomas.

AIMS OF THE STUDY: New motor deficit after surgery for deep-seated gliomas can occur from subcortical ischemia of the pyramidal tract. Motor evoked potentials (MEPs) validly indicate impending motor tract ischemia in cerebrovascular surgery. This study determines the feasibility and clinical utility of MEP monitoring for ischemic complication avoidance during surgery for deep-seated, specifically insular gliomas. METHODS: MEPs were recorded during 100 operations of insular gliomas. Intraoperative MEP results were correlated with postoperative clinical and imaging results. RESULTS: Useful MEP monitoring was possible in 89/100 cases, 88 of which were assessable since one patient died early postoperatively. Stable recordings warranted unimpaired motor outcome in 47/88 cases (53%). Surgical intervention reversed MEP attenuation in 26 of the remaining 41 cases (30% of the overall series) to prevent motor deficit except transient paresis in 12 (14%). Irreversible MEP changes without loss in eight cases (9%) resulted in only transient new deficit in seven cases, except one with permanent new paresis. Permanent paresis also occurred in seven cases (8%) where complete MEP loss could not be prevented. Permanent paresis arose exclusively through stroke of the deep motor pathways, whereas transient deficit typically corresponded to transitory ischemia of the pyramidal tract. MEP changes attributable to ischemic events frequently occurred spatially and temporally uncorrelated to resection in critical proximity of the motor tract. CONCLUSIONS: Ischemia in deep-seated glioma surgery usually occurs uncorrelated to resection close to the pyramidal tract. MEP monitoring efficiently helps detect ischemia early and to avert definite stroke and permanent new paresis in part of these cases.

Motor evoked potential monitoring for the surgery of brain tumours and vascular malformations.

Brain surgery incurs a significant risk of a new motor deficit in lesions within or adjacent to the motor areas and pathways which, for the patient, presents one of the most disabling complications of such operations. It is a major concern of intracranial procedures to delineate and monitor motor regions in order to preserve their structural and functional integrity, while still achieving maximal cytoreduction. The technique of motor evoked potential recording has had to be adapted to intraoperative recording conditions under general anaesthesia, but has been available for clinical use now for almost ten years. This contribution summarizes the current technique and related methods, as well as our clinical experience in some 400 cases of MEP monitoring in supratentorial tumors, lesions in and around the brainstem, and aneurysm surgery. Intraoperative MEP recordings have been shown to reliably reflect an impending new motor deficit. Irreversible MEP deterioration heralds new paresis, and unaltered recordings predict preserved motor function. This is also true in aneurysm surgery where conventional SEP monitoring may yield false-negative results with regard to development of a new motor deficit. Moreover, if MEP deterioration can be reversed, or halted by early surgical intervention, the presence of only a transient motor deficit, or even the lack of a new postoperative deficit, indicates the success of the MEP monitoring method in the prevention of a significant motor impairment. Certain complicated lesions can only be operated on at all because MEP monitoring is available. In conclusion, intraoperative MEP monitoring is a useful aid in brain surgery with which to avoid a new motor deficit without compromise to the surgical result. Controlled prospective studies will be required to verify the clinical value of the method.

Endocrinological outcome following first time transsphenoidal surgery for GH-, ACTH-, and PRL-secreting pituitary adenomas.

BACKGROUND: To study remission rates and pituitary functions following transsphenoidal surgery of newly diagnosed GH-, ACTH-, and PRL-secreting pituitary adenomas. METHODS: Out of a series of 329 newly diagnosed pituitary adenomas, 131 (39.8%) were hormone (67 GH-, 27 ACTH-, 37 PRL-) secreting. PRL-secreting adenomas were subjected to surgery because they failed to respond to previous medical treatment therapy. The data on secreting adenomas, regarding the results of standardised endocrinological testing, MRI findings and water metabolism disturbances, were extracted retrospectively from the pituitary data-base of the hospital. The mean follow-up was 3.7 years. RESULTS: The overall remission rate for PRL-secreting adenomas (27%) was significantly lower than for GH- (71.6%) and ACTH-secreting (81.5%) ones. Remission rates correlated negatively with the magnitude of preoperative hormone excess (not in Cushing's disease), tumour size (not in prolactinoma) and invasiveness. Generally, the improvement of the adenopituitary functions was statistically significant during the first three postoperative months, and thereafter remained unchanged. Diabetes insipidus persisting for more than three months occurred with similar frequency in the three patient groups (in 9.4% of GH-, in 6.7% of ACTH-, and in 10% of PRL-secreting adenomas). Tumour regrowth occurred more often in PRL-(20%) than in ACTH- (9.1%) and GH- (0%) secreting tumours. CONCLUSIONS: In GH- and ACTH-secreting pituitary adenomas, remission rates were significantly higher and recurrence rates lower than in PRL-secreting adenomas, which had failed to respond to previous medical therapy. The overall postoperative adenopituitary function was improved in all patient groups. Diabetes insipidus occurred with similar frequency in all patient groups. When reporting on results of surgery for secreting pituitary adenomas, not only remission and recurrence rates, but also the results of the pituitary function should be included.

Speaking modifies voice-evoked activity in the human auditory cortex.

The voice we most often hear is our own, and proper interaction between speaking and hearing is essential for both acquisition and performance of spoken language. Disturbed audiovocal interactions have been implicated in aphasia, stuttering, and schizophrenic voice hallucinations, but paradigms for a noninvasive assessment of auditory self-monitoring of speaking and its possible dysfunctions are rare. Using magnetoencephalograpy we show here that self-uttered syllables transiently activate the speaker's auditory cortex around 100 ms after voice onset. These phasic responses were delayed by 11 ms in the speech-dominant left hemisphere relative to the right, whereas during listening to a replay of the same utterances the response latencies were symmetric. Moreover, the auditory cortices did not react to rare vowel changes interspersed randomly within a series of repetitively spoken vowels, in contrast to regular change-related responses evoked 100-200 ms after replayed rare vowels. Thus, speaking primes the human auditory cortex at a millisecond time scale, dampening and delaying reactions to self-produced "expected" sounds, more prominently in the speech-dominant hemisphere. Such motor-to-sensory priming of early auditory cortex responses during voicing constitutes one element of speech self-monitoring that could be compromised in central speech disorders.