Absence Of Cortical Responses Research Articles

Neurological and Hematological Recovery Following Copper Replacement in Severe Copper Deficiency-induced Myelopathy and Cytopenia

Background: Copper deficiency can lead to a severe myelopathy and cytopenia. The myelopathy can lead to inability to walk by paresis and deafferentation. The anemia can as well be severe with the need for blood transfusions. Beside innate reasons it occurs years after surgeries of the intestine and following disturbed resorption. It can also occur due to excessive intake of zinc that binds copper. An early diagnosis following copper substitution can lead to restitution. It can clinically be mistaken for a vitamin B12 deficiency. This circumstance can lead to a delayed treatment. Case: A 67 years old woman with severe gait disturbances, sensory ataxia was admitted to our hospital. She had the diagnosis of vitamin B12 deficiency. B12 was elevated and metabolites were in normal range. The electrophysiology showed a deafferentation of the legs. Objective: This case report provides detailed information about the course of diagnosis and the treatment of a severe copper deficiency with symptomatic myelopathy and cytopenia in an elderly woman. Methods: We performed a literature research with keywords “spinal cord disease, gait disturbances, elevated lactate in cerebrospinal fluid, anemia”. We did blood tests and CSF on a regular basis combined with clinical assessments and electrophysiology. Results: Serum copper was not detectable. CSF copper was reduced (8.7 µg/l, Ref.: 14.2-109 µg/l), CSF lactate was elevated (4.69 mmol/l, Ref.: 1.1-2.4 mmol/l). The patient had a cytopenia (Hb 6.6 g/dl, Ref.: 12-16 g/dl, MCV 130 fl, Ref.: 80-96 fl, leucocytes 2.3 10³, Ref.: 4.3-10 10³/µl). Vitamin B12 amounted to 891 pg/ml (Ref.: 191-663 pg/ml). The somatosensory evoked potential (SEP) study showed absent cortical responses after stimulation of the sural nerves bilaterally. Due to the diagnosis of a myelopathy and bone marrow dysfunction due to copper deficiency we substituted copper-histidine subcutaneously. This led to a marked improvement of symptoms, an increase of serum copper levels (141 µg/l), CSF copper levels (14.1 µg/l), hemoglobin (11.9 g/dl), leukocyte count (11.4 10³/µl) and a normalization of CSF lactate. Conclusion: Elevated CSF lactate might be an indicator for treatable myelopathy due to copper deficiency in patients with afferent gait disturbances. A timely substitution can lead to a marked improvement of even severe symptoms.

Subjective and Objective Assessments of Post-traumatic Olfactory Dysfunction.

Introduction: Traumatic brain injuries are the most common cause of olfactory dysfunction. Deficits in olfaction may be conductive or neurosensory in nature, with varying degrees of impairment resulting in a diminished quality of life and an increased risk for personal injury among patients. The aim of this research is to evaluate the results of the subjective and objective quantitative examinations of olfactory function in a group of patients with post-traumatic anosmia in order to predict its value in identifying olfactory deficits in clinical practice.Materials and Methods: The present study included 38 patients who reported anosmia or hyposmia caused by a traumatic head injury, and a group of 31 age- and sex-matched controls without olfactory dysfunction or prior history of head injury. The comparison of odor perception and identification of two oils (mint and anise) was assessed with the use of blast olfactometry with cortical olfactory event-related potentials.Results: Subjective olfactory tests revealed anosmia or hyposmia in 94% of patients with head injury-related olfactory dysfunction. Objective tests revealed olfactory event-related potentials from cranial nerve I produced by the stimulation with both mint and anise in 20 patients (52.6%). Olfactory event-related potentials from cranial nerve V produced by the stimulation with mint were registered in 26 patients (68.4%). The lack of any responses, from both cranial nerve I and V, was found in 12 patients (32% of cases).Conclusions: Findings from our study indicate the application of both subjective and objective examinations in the evaluation of patients with olfactory impairment. In the diagnosis of post-traumatic anosmia or hyposmia, objective examinations are particularly useful when the patients' level of cognition may be impaired or when subjects may be exaggerating their olfactory defects for a secondary gain. The diagnosis of damage to the olfactory system, specifically in the receptive part of the olfactory pathway, can be established in patients who showed reduced amplitudes or absent cortical responses in addition to absent odor identification and perception threshold in the subjective examination.

Inter-predictability of Neuroprognostic Modalities After Cardiac Arrest.

IntroductionAt present, there is an emphasis on a multi-modal approach to neuro-prognostication after cardiac arrest using clinical examination, neurophysiologic testing, laboratory biomarkers, and radiological studies. However, this necessitates significant resource utilization and can be challenging in under-resourced clinical settings. Hence, we sought to determine the inter-predictability and correlation of prognostic tests performed in patients after cardiac arrest.MethodsFifty patients were included through neurophysiology laboratory data for this retrospective study. Clinical, radiological and neurophysiological data were collected. Neurophysiological data were re-evaluated by a board-certified neurophysiologist for the purpose of the study. Chi-square testing was used to evaluate the correlation between different diagnostic modalities.ResultsWe found that a non-reactive electroencephalogram (EEG) had a predictive value of 79% for absent bilateral cortical responses (N20) with somatosensory evoked potentials (SSEP). On the other hand, absent bilateral cortical responses N20 had 87% predictive value for a non-reactive EEG. Also, absent cortical responses and non-reactive EEG had predictive values of 78% and 72% for anoxic injury on magnetic resonance imaging (MRI) brain respectively with a non-significant difference on chi-square testing. Individually, absent bilateral N20 SSEP, a non-reactive EEG and anoxic brain injury on MRI studies were highly predictive of poor outcome [modified Rankin scale (mRS) > 4] at hospital discharge.ConclusionNeuroprognostication in a post-cardiac arrest setting is often limited by self-fulfilling prophecy. Given the lack of absolute correlation between different modalities used in post-cardiac arrest patients, the value of the multi-modal approach to neuro-prognostication is highlighted by this study.

Pelvic floor electrophysiology in spinal cord injury.

The study aimed to investigate sacral peripheral nerve function and continuity of pudendal nerve in patients with chronic spinal cord injury (SCI) using pelvic floor electrophysiological tests. Twelve patients with low cervical or thoracic SCI were prospectively included. Quantitative external anal sphincter (EAS) muscle electromyography (EMG), pudendal nerve terminal motor latency (PNTML) testing, bulbocavernosus reflex (BCR) testing and pudendal short-latency somatosensory-evoked potential (SEP) measurement were performed. In EAS muscle EMG, two patients had abnormal increased spontaneous activity and seven prolonged motor unit potential duration. PNTML was normal in 10 patients. BCR was present with normal latency in 11 patients and with prolonged latency in one. The second component of BCR could be recorded in four patients. SEPs showed absent cortical responses in 11 patients and normal latency in one. Pudendal nerve and sacral lower motor neuron involvement are significantly associated with chronic SCI, most prominently in EAS muscle EMG. The frequent finding of normal PNTML latencies supports earlier concerns on the utility of this test; however, BCR and pudendal SEPs may have clinical relevance. As intact peripheral nerves including pudendal nerve are essential for efficient supportive therapies, pelvic floor electrophysiological testing prior to these interventions is highly recommended.

Cardiac Arrest and Postanoxic Encephalopathy.

Neuroprognostication following cardiac arrest is a common and challenging dilemma for neurologists and intensivists, complicated by the use of therapeutic hypothermia and targeted temperature management. Great advances have been made in understanding the mechanisms of disorders of consciousness in hypoxic-ischemic brain injury, and new diagnostic and therapeutic avenues are arising. In the era of therapeutic hypothermia and targeted temperature management, traditional clinical signs, electrophysiologic findings, and chemical biomarkers have now become questionable or variable, and the proper time for diagnostic and prognostic testing has become murky. Although the value of absent pupillary and corneal reflexes remains fairly robust, the presence of myoclonic status epilepticus and a motor response of extensor posturing or worse no longer appear to have acceptable false-positive rates. Somatosensory evoked potentials (SSEPs), thought to be the most reliable ancillary test for predicting prognosis, have recently been the subject of several reports showing unexpectedly good outcome in the face of absent cortical responses. The presence or absence of reactivity on EEG appears to be a promising prognostic sign, and aggressive treatment of seizures (and even status epilepticus) may lead to better than expected outcomes. Serum biomarkers that were previously felt to be valid, such as elevated neuron-specific enolase, have been drawn into question owing to multiple reports of patient survival with good outcome despite highly elevated levels. Advanced EEG and neuroimaging techniques, particularly looking at functional connectivity and underlying neuronal pathways, are giving great insights to the underlying mechanisms of disease and potential therapeutic targets. Predicting neurologic prognosis following cardiac arrest is an evolving field, with new prognostic methods and reevaluation of older techniques holding great promise for advancing our ability to predict outcome and improve patient care.

Cognitive auditory evoked potentials in coma: can you hear me?

This scientific commentary refers to ‘Neural detection of complex sound sequences in the absence of consciousness’, by Tzovara et al. (doi:10.1093/brain/awv041). Event related potentials (ERPs), classically measured by EEG, are the electrophysiological brain responses to a stimulus. Somatosensory and auditory ERPs have been used as a non-invasive tool for assessing brain functions and predicting outcomes in disorders of consciousness and coma (for review see Bruno et al. , 2011). While early ERPs (such as the absence of cortical responses on somatosensory-evoked potentials) predict poor outcomes, cognitive ERPs may be indicative of recovery of consciousness after coma (Vanhaudenhuyse et al. , 2008). Auditory cognitive ERPs permit assessment of residual higher-order processing, such as echoic memory (e.g. using mismatch negativity potentials), acoustic and semantic discrimination (e.g. P3 or P300 evoked potentials), and incongruent language detection (e.g. N400 potentials). Classically, these ERP paradigms are based on the detection of a stimulus in violation of an auditory regularity, composed of two neural events, each characterized at the EEG level by a stereotypical morphology and latency: a mismatch negativity followed by a later complex named P300 further divided into an early (P300a) and a late component (P300b). The mismatch negativity is thought to reflect unconscious processing (Daltrozzo et al. , 2009), whereas the P300b has been linked to consciousness (Bekinschtein et al. , 2009). Neither of these ERP components are specific to auditory stimuli and both can be elicited by other sensory modalities. However, auditory cognitive ERPs have been used most extensively in the field of coma because they are easy to deliver and—in contrast to visual ERPs—can be easily acquired in eyes closed conditions. Given the …

Hypoxic-Ischemic Brain Injury and Prognosis After Cardiac Arrest

: Cardiac death is the leading cause of death in the United States, and patients who have out-of-hospital cardiac arrest have only a 1% to 10% survival rate, despite improvements in advanced life support. The neurologic sequelae of hypoxic-ischemic brain injury after cardiac arrest vary from subtle cognitive impairment to coma, persistent vegetative state, and brain death. Neurologists are commonly asked to prognosticate neurologic outcome after cardiac arrest. : In 2002, two randomized controlled trials demonstrated that therapeutic hypothermia (32°C to 34°C [89.6°F to 93.2°F]) increases the odds of improved neurologic outcome and reduces the risk of death compared with normothermia when applied for the initial 12 to 24 hours after ventricular fibrillation or tachycardia cardiac arrest. Considerable research continues into neurologic prognostication after hypoxic-ischemic brain injury, especially with the advent of therapeutic hypothermia and its effects on the clinical examination, neurophysiologic studies, and serum biomarkers of brain injury. Recent reports indicate that poor motor response 72 hours after cardiac arrest, absent cortical responses on median nerve somatosensory-evoked potentials, and elevated neuron-specific enolase may not necessarily indicate poor prognosis in patients treated with therapeutic hypothermia compared with historical populations not treated with hypothermia, perhaps because of sedation and neuromuscular blockade. : Neurologic prognostication after cardiac arrest remains challenging because of the sedation and neuromuscular blocking agents given to patients who undergo therapeutic hypothermia. A multimodal algorithmic approach (clinical, electrophysiologic, and possibly serum biomarker testing) is suggested for cardiac arrest patients treated with hypothermia, but further research is needed to determine more accurate prognostic predictors.

Sedation Confounds Outcome Prediction in Cardiac Arrest Survivors Treated with Hypothermia

Therapeutic hypothermia is commonly used in comatose survivors' post-cardiopulmonary resuscitation (CPR). It is unknown whether outcome predictors perform accurately after hypothermia treatment. Post-CPR comatose survivors were prospectively enrolled. Six outcome predictors [pupillary and corneal reflexes, motor response to pain, and somatosensory-evoked potentials (SSEP) >72 h; status myoclonus, and serum neuron-specific enolase (NSE) levels <72 h] were systematically recorded. Poor outcome was defined as death or vegetative state at 3 months. Patients were considered "sedated" if they received any sedative drugs ≤ 12 h prior the 72 h neurological assessment. Of 85 prospectively enrolled patients, 53 (62%) underwent hypothermia. Furthermore, 53 of the 85 patients (62%) had a poor outcome. Baseline characteristics did not differ between the hypothermia and normothermia groups. Sedative drugs at 72 h were used in 62 (73%) patients overall, and more frequently in hypothermia than in normothermia patients: 83 versus 60% (P = 0.02). Status myoclonus <72 h, absent cortical responses by SSEPs >72 h, and absent pupillary reflexes >72 h predicted poor outcome with a 100% specificity both in hypothermia and normothermia patients. In contrast, absent corneal reflexes >72 h, motor response extensor or absent >72 h, and peak NSE >33 ng/ml <72 h predicted poor outcome with 100% specificity only in non-sedated patients, irrespective of prior treatment with hypothermia. Sedative medications are commonly used in proximity of the 72-h neurological examination in comatose CPR survivors and are an important prognostication confounder. Patients treated with hypothermia are more likely to receive sedation than those who are not treated with hypothermia.

ETHICAL DILEMMAS IN THE NEUROLOGIC ICU

ETHICAL DILEMMAS IN THE NEUROLOGIC ICU

Prognostic value of brain diffusion‐weighted imaging after cardiac arrest

Outcome prediction is challenging in comatose postcardiac arrest survivors. We assessed the feasibility and prognostic utility of brain diffusion-weighted magnetic resonance imaging (DWI) during the first week. Consecutive comatose postcardiac arrest patients were prospectively enrolled. AWI data of patients who met predefined specific prognostic criteria were used to determine distinguishing apparent diffusion coefficient (ADC) thresholds. Group 1 criteria were death at 6 months and absent motor response or absent pupillary reflexes or bilateral absent cortical responses at 72 hours or vegetative at 1 month. Group 2 criterion was survival at 6 months with a Glasgow Outcome Scale score of 4 or 5 (group 2A) or 3 (group 2B). The percentage of voxels below different ADC thresholds was calculated at 50 x 10(-6) mm(2)/sec intervals. Overall, 86% of patients underwent DWI. Fifty-one patients with 62 brain DWIs were included. Forty patients met the specific prognostic criteria. The percentage of brain volume with an ADC value less than 650 to 700 x 10(-6)mm(2)/sec best differentiated between Group 1 and Groups 2A and 2B combined (p < 0.001), whereas the 400 to 450 x 10(-6)mm(2)/sec threshold best differentiated between Groups 2A and 2B (p = 0.003). The ideal time window for prognostication using DWI was between 49 and 108 hours after the arrest. When comparing DWI in this time window with the 72-hour neurological examination, DWI improved the sensitivity for predicting poor outcome by 38% while maintaining 100% specificity (p = 0.021). Quantitative DWI in comatose postcardiac arrest survivors holds promise as a prognostic adjunct.

Does Stimulus Rate Matter When Performing Somatosensory Evoked Potentials for Coma Patients?

It is unclear whether the rate of stimulation for somatosensory evoked potentials (SEPs) can influence the presence or absence of cortical responses to median nerve stimulation in comatose patients. If so, this could affect how SEPs are performed and interpreted for prognostication in coma. Our objective was to determine how frequently our comatose patients had absent median nerve SEP responses at 3 Hz stimulation, but present responses at 1 Hz stimulation, and to report outcomes of these patients. We reviewed SEP recordings in 639 comatose patients over a 9-year period. All had stimulation at 3 Hz and 1 Hz. This is a retrospective review. There were seven patients who had absent median nerve SEP responses at 3 Hz stimulation bilaterally, but had present responses at 1 Hz on one or both sides. Six of the seven died. One 16-year-old patient with traumatic brain injury awoke, but had moderate disability. Stimulation rate is an important determinant of presence or absence of cortical responses in about 1% of comatose patients. It is unclear whether such patients have a different outcome that those with absent responses at both rates of stimulation.

Cognitive Event-Related Potentials in Comatose and Post-Comatose States

We review the interest of cognitive event-related potentials (ERPs) in comatose, vegetative, or minimally conscious patients. Auditory cognitive ERPs are useful to investigate residual cognitive functions, such as echoic memory (MMN), acoustical and semantic discrimination (P300), and incongruent language detection (N400). While early ERPs (such as the absence of cortical responses on somatosensory-evoked potentials) predict bad outcome, cognitive ERPs (MMN and P300) are indicative of recovery of consciousness. In coma-survivors, cognitive potentials are more frequently obtained when using stimuli that are more ecologic or have an emotional content (such as the patient's own name) than when using classical sine tones.

Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review) [RETIRED

To systematically review outcomes in comatose survivors after cardiac arrest and cardiopulmonary resuscitation (CPR). The authors analyzed studies (1966 to 2006) that explored predictors of death or unconsciousness after 1 month or unconsciousness or severe disability after 6 months. The authors identified four class I studies, three class II studies, and five class III studies on clinical findings and circumstances. The indicators of poor outcome after CPR are absent pupillary light response or corneal reflexes, and extensor or no motor response to pain after 3 days of observation (level A), and myoclonus status epilepticus (level B). Prognosis cannot be based on circumstances of CPR (level B) or elevated body temperature (level C). The authors identified one class I, one class II, and nine class III studies on electrophysiology. Bilateral absent cortical responses on somatosensory evoked potential studies recorded 3 days after CPR predicted poor outcome (level B). Burst suppression or generalized epileptiform discharges on EEG predicted poor outcomes but with insufficient prognostic accuracy (level C). The authors identified one class I, 11 class III, and three class IV studies on biochemical markers. Serum neuron-specific enolase higher than 33 microg/L predicted poor outcome (level B). Ten class IV studies on brain monitoring and neuroimaging did not provide data to support or refute usefulness in prognostication (level U). Pupillary light response, corneal reflexes, motor responses to pain, myoclonus status epilepticus, serum neuron-specific enolase, and somatosensory evoked potential studies can reliably assist in accurately predicting poor outcome in comatose patients after cardiopulmonary resuscitation for cardiac arrest.

Lower urinary tract dysfunction in Machado–Joseph disease: a study of 11 clinical-urodynamic observations

Objectives: Machado–Joseph disease (MJD), or hereditary spinocerebellar ataxia type 3, is the most common dominantly inherited ataxia. However, lower urinary tract (LUT) dysfunction in MJD has not been fully delineated. We investigated LUT dysfunction in MJD by clinical-urodynamic observations. Methods: In 24 genetically diagnosed MJD, we recruited all 11 patients with LUT symptoms (six men, five women; age, 18–61 [mean 48] years; disease duration, 2–24 [mean 9] years; voiding difficulty, 7, urinary incontinence, 4). Urodynamic studies consisted of uroflowmetry, measurement of post-void residuals and electromyography (EMG)-cystometry. Neurophysiology tests consisted of motor unit potential (MUP) analysis of the sphincter and extremity muscles, tibial nerve somatosensory evoked potentials (SEP) and nerve conduction studies (NCS) of the extremities. Results: Urodynamic abnormalities were seen in all 11 patients studied. Maximum or average flow rate was decreased in five. Post-void residual was noted in three but residual urine volume >100 ml was noted in only one patient. Maximum urethral closure pressure was low in one and high in one of five patients studied. EMG-cystometry during filling showed detrusor overactivity in five, impaired bladder sensation in four, low compliance detrusor in one, uninhibited sphincter relaxation in one and incompetent urethra in one. Voiding phase abnormalities included detrusor areflexia in three and detrusor-sphincter dyssynergia in two. Bethanechol supersensitivity of the bladder was noted in one of three patients studied. Bulbocavernosus reflex was absent in two of five patients studied. MUP analysis showed neurogenic changes in six of nine sphincter muscles and in all six extremity muscles studied. Five patients had prolonged or absent cortical response in SEP and four had sensory axonal neuropathy in NCS, which were relevant to the impaired bladder sensation. Conclusion: In the present study, a half of MJD patients had LUT symptoms and they showed various urodynamic abnormalities. Detrusor overactivity, impaired bladder sensation, and neurogenic sphincter EMG were common findings, and large post-void residuals were rare. These findings are relevant to central and peripheral nervous system pathology of MJD.

Early recovery after closed traumatic head injury: somatosensory evoked potentials and clinical findings.

To determine the ability of somatosensory evoked potentials (SEP) compared with clinical findings to monitor and predict recovery in patients suffering from closed head injury with predominantly diffuse axonal injury (DAI). Prospective cohort study. Neurologic intensive care unit (ICU) of a university hospital. Serial SEP recordings were obtained from 31 consecutive patients with closed head injury. The first SEP was recorded within 48 hrs after trauma, followed by recordings after another 2 days, after which the time interval for each consecutive recording was doubled. Clinical examinations were performed every 6 hrs during the ICU stay and daily after transfer to a general neurologic ward. None. Twenty-three of 31 patients demonstrated pathologic SEP findings at initial examination. Of these patients, 11 recovered clinically, two remained vegetative, and ten died. In all 11 patients with clinical recovery, SEP also recovered. In 8 of 31 patients, initial SEPs were normal and remained normal until discharge, all eight had a good outcome. Initial SEP findings were related with outcome at 6 months (p = .02), and follow-up studies increased the predictive value of SEP studies (p = .009). Other factors related to outcome included age, severity of DAI, and length of ICU/hospital stay. In the 11 patients with SEP and clinical recovery, early (day 2) and late (>or=2 months) recovery was documented. Early and reliable SEP indicators of improvement included N20-P25-Amplitudes (mean recovery, 8.5 days) and central conduction time (9.6 days). Pupillary light reaction (6.4 days), Babinski reflex (12.4 days), and Glasgow Coma Score (9.6 days) were the most valuable clinical findings. Recovery of the Glasgow Coma Score frequently coincided with reduction of sedatives. In most patients, recovery was detected with SEP before clinical recovery (7/11 patients, time difference 1 wk). Initial SEP findings correlate with long-term outcome in patients with closed head injury with DAI. Initial bilaterally absent cortical responses in the SEP reliably predicted death, whereas completely normal SEP findings predicted good long-term outcome. Early recovery after DAI can be detected with serial SEP recordings despite sedative medications. Electrophysiologic recovery frequently precedes clinical recovery.

Topographical features of the sensory-evoked responses in malformed brains

To reveal the functional organization of the somatosensory area in the dysgenetic cortex, somatosensory-evoked potentials were examined in seven patients with congenital brain anomalies diagnosed by magnetic resonance imaging, including six patients in whom multichannel recordings over the scalp were used. In four patients with polymicrogyria/pachygyria and two with lissencephaly, the early cortical responses, frontal P20 and parietal N20, were absent in the cortex contralateral to the stimulated side. The first cortical response was a positive wave that appeared predominantly over the centroparietal area in five patients, and in the frontal area in the other patient with polymicrogyria/pachygyria. These findings suggest that the differentiated somatosensory function is distributed normally in the centroparietal cortex in most cases of widespread cortical dysplasia. However, the absence of P20/N20 may indicate a hypoplastic central sulcus or functionally undifferentiated subdivision of the somatosensory cortex in these patients. The absence of cortical responses in the patient with holoprosencephaly may correspond with growth failure of the thalamocortical afferent projections in this disorder.

Detection of nontraumatic comatose patients with no benefit of intensive care treatment by recording of sensory evoked potentials.

To determine the predictive ability of sensory evoked potential recordings in nontraumatic comatose patients. To evaluate the hypothesis that patients with bilateral absent cortical responses ultimately die despite long-term intensive care treatment. Prospective cohort study. Medical intensive care unit (ICU) of a university hospital. Four hundred forty-one adult nontraumatic comatose patients (unarousable unresponsiveness to external stimulation, Glasgow Coma Score < or = 7) from various causes. Six hundred seventy-six sensory evoked potential measurements were performed within 7 days after onset of coma. Death or survival to hospital discharge. Eighty-six patients (20%) had a bilateral loss of the cortical evoked potential N20 peak. Despite long-term intensive care treatment, all died without awakening from coma (mortality rate, 100%; 95% confidence interval, 96-100). The mean stay at the ICU after evoked potential measurement until death was 8.1 days (697 patient days). The overall cost of ICU management for these 86 patients accounted for approximately $1,324,300. In the remaining 355 comatose patients with preserved cortical N20 peak, 148 (42%) survived and 207 (58%) died. In this latter group of patients, cervicomedullary N13 to cortical N20 conduction time was prolonged in nonsurvivors (mean +/- SD, 6.7 +/- 1.3 milliseconds) compared with that in survivors (mean +/- SD, 6.4 +/- 1.2 milliseconds, P < .05) and healthy controls (mean +/- SD, 5.5 +/- 0.4 milliseconds, P < .05). Although this difference is statistically significant, a preserved N20 peak is not useful to discriminate whether the individual patient will survive (N13-N20 conduction time of > 7 milliseconds had a positive predictive value of correct prediction of death of 0.67). Recording of sensory evoked potentials identifies a subgroup of adult nontraumatic comatose patients with a mortality rate of 100% in our sample. In these patients, advanced intensive care treatment should be withdrawn to provide limited ICU resources for patients with higher probability of favorable outcome. We emphasize that these results are not applicable to comatose patients following closed head trauma and particularly not to children.

Somatosensory evoked potentials and outcome in perinatal asphyxia.

Somatosensory evoked potentials (SEP) can be measured in the term newborn infant and given an index of function in the areas of the brain most likely to be damaged in perinatal asphyxia. We studied the median nerve SEP in 30 asphyxiated term infants over the course of their encephalopathy and until discharge from the neonatal unit. Three types of response were noted: normal waveform, abnormal waveform, or absence of cortical response. Follow up of the survivors was undertaken at a mean age of 12 months by means of a Griffiths' assessment and neurological examination. Nine infants died of their asphyxial illness and one of spinal muscular atrophy. Of the 20 survivors, three have cerebral palsy, four have minor abnormalities, and 13 are neurodevelopmentally normal. There was a close correlation between outcome and SEP. All 13 infants with normal outcome had normal SEP by 4 days of age, whereas those with abnormal or absent responses beyond 4 days had abnormalities at follow up.

Somatosensibel und motorisch evozierte Potentiale bei der prognostischen Beurteilung traumatisch und nichttraumatisch komatöser Patienten

Somatosensory evoked potentials have proved to be useful for the outcome prediction of comatose patients. To date there are no reliable data with the investigation of motor evoked potentials (MEP) in this question. In the present study 60 patients with traumatic (group I) and 35 with non-traumatic coma (group II) were examined with both electrophysiological tests. It was the aim of this study to find out whether additional recording of MEP could contribute to a better prediction of the outcome than SEP alone. Our results clearly indicate that in terms of prognostic value SEP are superior to MEP. All patients with bilaterally preserved SEP and a central conduction time ≤ 6.5 msec (SEP-type la) survived whereas all patients with bilaterally absent cortical responses (SEP-type III) died. On the other hand, 12 patients (30.7 %) of group I and 11 patients (39.3 %) of group II with bilaterally preserved electromyographic responses following transcranial stimulation (MEP-type I) died. Only the bilateral absence of MEP (type III) was an unerring unfavourable prognostic sign. On the whole, we cannot recommend the use of MEP in prognostic evaluation of comatous patients.

Prognostic utility of SEPs in comatose children

Somatosensory evoked potentials (SEPs) were recorded in 73 comatose children upon admission to the intensive care unit and were studied in respect to initial neurologic status and final outcome. SEP results were graded normal, increased interpeak latencies, and unilaterally or bilaterally absent cortical responses. Of the 50 patients with Glasgow Coma Scale scores less than 7 upon admission, only 3 had SEPs within the normal range, while 37 had unilaterally or bilaterally absent SEPs. None of the 27 who died had normal SEPs; 1 had increased interpeak latencies, 26 had more abnormal SEPs. The 14 with normal outcomes had normal (9 patients) or delayed (4 patients) SEPs; the latter group returned to normal within a few days. Repeat SEP studies were performed in 33 patients. SEPs were relatively stable during the intensive care observation, with the exception of 6 patients with Reye syndrome. Subsequent studies are recommended in all patients, but are essential in those with Reye syndrome in order to be useful prognostically. The utility of SEPs did not vary as a function of coma etiology. These data support the usefulness of SEPs in early prediction of neurologic outcome in comatose children.