Preserved cortical somatosensory evoked potentials in apnoeic coma with loss of brain-stem reflexes: case report

A comatose patient suffering from diffuse cerebellar haemorrhage developed apnoea and brainstem areflexia, i.e. the clincial signs of brain death. However, median nerve somatosensory evoked potential testing 2.5 h and 22 h after the onset of this clinical syndrome showed cortical potentials partly preserved; these were abolished 46 h after the beginning of the clinical signs of brain death. This case report underlines the need for electrophysiological confirmation of brain death in patients with primarily infratentorial lesions.     

Short- and long-latency median somatosensory evoked potentials. Findings in patients with localized neurological lesions

Short- and long-latency somatosensory evoked potentials (SEPs) were elicited by stimulation of the median nerve in 43 patients with neurological disorders. Abnormalities of short-latency peaks, P9, N13, and P14, were seen in patients with lesions of the peripheral nerve, cervical spinal cord, and brain stem, respectively. Subsequent component, N18, was affected in patients with thalamic or hemispheric disease. In some patients with parietal lobe lesions, however, abnormalities were limited to later components, N32 or N63. Analysis of SEPs is helpful in localizing a lesion along the somatosensory pathway, although differentiation between thalamic and other subcortical or cortical involvement may not be possible with the present SEP technique. Both short- and long-latency SEPs should be studied for maximal clinical information. The latter can be most reliably evaluated by simultaneous bilateral stimulation.     

Cranial muscle activity in dissociated brain death

The origin of spontaneous myogenic activity during the registration of isoelectric EEGs for documentation of total brain death has not yet been explained. In nine patients with total brain death, completely abolished acoustic evoked brainstem potentials (AEP), somatosensory evoked potentials (SEP) as well as electrically evoked blink-reflexes (BR) were demonstrated. The peripheral conduction capacity of the facial nerve, however, was never impaired. These findings suggest that peripheral nerve function may be well preserved although brain stem activity is completely abolished and therefore support the thesis that the myogenic activity in cranial muscles in total brain death is not mediated by the brain stem but is of extracerebral origin.     

EEG and evoked potentials in comatose patients with severe brain damage

EEGs and evoked potentials were recorded in 76 deeply comatose and unresponsive patients with traumatic or non-traumatic cerebral damage. Spontaneous EEG activity was absent in 37 of the patients on the initial examination. The cortical somatosensory evoked potentials were invariably absent in these patients as were the visual evoked potentials. Brain-stem evoked potentials were abnormal, either lacking all waves or with only wave I or II present. Cerebral angiography performed in 33 of the patients within minutes to a few hours after the neurophysiological examination verified an established brain death, showing full intracerebral circulatory arrest in all. Spontaneous EEG activity was initially present in 32 patients on the first examination, 20 of whom had bilaterally abolished cortical somatosensory potentials. Ten of the patients died a few hours after the initial examination, another 10 were followed for 2-3 days and subsequently developed electrocortical silence (ECS). Twelve of the patients with spontaneous EEG activity had preserved cortical somatosensory potentials, either uni- or bilaterally. The only two who survived were found in this group. In the patients followed with multiple recordings over a few days, the first parameter to indicate a grave prognosis was always disappearance of the cortical somatosensory potentials bilaterally, which generally occurred hours, and sometimes a day or two, before cessation of the spontaneous EEG activity. EEG records from 7 patients did not meet the technical criteria of ECS; all, however, had abolished cortical somatosensory potentials bilaterally, and none in this group survived.     

The value of ulnar somatosensory evoked potentials (SEPs) in cervical myelopathy

In 57 patients with clinical signs and surgical documentation of compressive myelopathy, ulnar nerve somatosensory evoked potentials (SEPs) were more sensitive (with 74% abnormal) than either median or tibial nerve SEPs. The most frequent abnormalities were reduced or absent neck evoked responses and prolonged central conduction time. All subjects who had an SEP abnormality were identified by combined tibial and ulnar SEPs. Median nerve SEP added no additional information. Normal ulnar and tibial nerve SEPs were also able to exclude major cord damage in patients with cervical radiculopathy but little evidence of myelopathy.     

Short- and long-latency tibial somatosensory evoked potentials in cerebral lesions affecting rolandic leg areas

Summary Short- and long-latency tibial somatosensory evoked potentials (SEPs) were studied in nine patients with clinical presentation primarily involving one lower extremity. In group 1, with extensive infarcts in the territory of anterior cerebral artery, tibial cortical SEPs were uniformly absent. In group 2, with small infarcts involving Rolandic leg areas, tibial SEPs showed a decrease in overall response amplitude and attenuation of P40. In group 3, with discrete mass lesions compressing Rolandic leg areas, P40 was preserved but might be delayed. Late SEP components (N75, P100 and N135) tended to be preserved in the patients of group 2 and 3. The data suggest that Rolandic leg areas and the neighboring cortex are crucial for short- and long-latency tibial cortical SEPs and that small lesions affecting Rolandic leg areas tend to affect short-and mid-latency SEP components.     

Serial median nerve SEPs and SSEPs in patients with West syndrome

We studied serial median nerve somatosensory evoked potentials (SEPs) and short latency somatosensory evoked potentials (SSEPs) in 17 patients with West syndrome. Four of the 7 patients with absent SEPs in the initial examination showed recognizable SEPs in the follow-up studies, associated with improvement of electroencephalogram (EEG). This indicated that SEPs were variable with condition of epilepsy and lack of initial SEPs was not always a poor prognostic factor for seizure control and developmental outcome. Persistent lack of SEPs, however, indicated poor outcome of seizures, EEG and development. Central conduction time in SSEPs did not correlate with seizure or developmental outcome.     

Tumors localized near the central sulcus may cause increased somatosensory evoked potentials.

OBJECTIVE: Median nerve somatosensory evoked potentials (SEPs) may be altered in patients with cerebral tumors. In rare cases cortical responses may be increased, but the significance of this finding remains unclear. METHODS: We investigated 3 patients in whom an epileptic seizure was the only neurological symptom of a cerebral tumor located near the central sulcus. We studied median nerve SEPs, motor evoked potentials in abductor digiti minimi muscle, and long-loop reflexes in abductor pollicis brevis muscle bilaterally. Two patients also underwent intraoperative neurophysiological monitoring. RESULTS: All 3 patients presented with enlarged cortical SEPs on the side of the brain tumor. The responses increased further post-operatively, and the enhancement persisted in follow-up examinations up to 6 months after surgical tumor extirpation. Intraoperative monitoring documented a substantial increase of the enlarged potential N20-P22 during tumor removal in one patient, who also presented with an exaggerated long-loop reflex on the tumor side. Transcranial magnetic stimulation revealed unremarkable motor evoked potentials in all 3 patients. CONCLUSIONS: Distinct mechanisms must be considered in order to explain both immediate and long-term changes of neuronal excitability leading to increased cortical SEPs. SIGNIFICANCE: Hyperexcitability of cortical neurons or insufficient cortical inhibitory mechanisms may be responsible for increased SEPs, which may serve as an epileptic marker in patients suffering from a tumor near the central sulcus.     

Multimodality evoked potentials and brain death. Prerequisites, findings and problems

According to the recommendations of the medical board of the FRG the clinical diagnosis of cerebral death in adults requires an observation period of 12 hours. Evoked cerebral potentials have been accepted as a technical method of confirmation of clinical signs. In 32 patients with the signs of apneic brain-stem areflexia acoustic evoked brain-stem potentials and median-evoked somatosensory potentials were recorded. In supratentorial lesions evoked potentials are adequate to confirm complete cessation of brain function. In three cases of primary brain-stem disease evoked potentials were abolished, however, unequivocal EEG activity was preserved. The registration of evoked potentials is sufficient to confirm the brain death syndrome in primary supratentorial lesions, in infratentorial disease, however, demonstration of isoelectric EEG is necessary.     

Central motor and sensory conduction in X-linked recessive bulbospinal neuronopathy.

Central conduction was studied in 12 patients with X-linked recessive bulbospinal neuronopathy (XBSN) using percutaneous electrical cortical, cervical and lumbar stimulation and somatosensory evoked potentials (SEPs). The central motor conduction time from the motor cortex to the cervical and lumbar segments of the spinal cord was normal in XBSN. SEPs, however, were abnormal or central sensory conduction time was prolonged in patients with XBSN. These results are consistent with the clinicopathological findings of XBSN in which the primary sensory neurons are involved as well as the lower motor neurons in the CNS, whereas the upper motor neurons are well preserved.     

Brain function in patients with cerebral fat embolism evaluated using somatosensory and brain-stem auditory evoked potentials

Summary In two victims of traffic accidents with broken bones and fat embolism, serial recordings of somatosensory evoked potentials (SEPs) and brain-stem auditory evoked potentials (BAEPs) were examined to assess brain function. Initial SEPs and BAEPs revealed normal subcortical components, while the late cortical components of SEPs were abolished, findings indicative of diffuse dysfunction of grey rather than of white matter. As the neurological functions became normal, the late components appeared. It is concluded that while absent late components of SEPs do reflect cortical dysfunction, they are not necessarily associated with a poor prognosis. Repetitive recordings of SEPs appear to be a useful tool for assessing the neurological condition and the prognosis of patients with cerebral fat embolism.     

Evoked potentials in olivopontocerebellar atrophy

Pattern-reveral visual evoked potentials, far-field and cortical somatosensory evoked potentials, and auditory brainstem potentials were recorded in two patients with olivopontocerebellar atrophy. In one patient, visual evoked potentials exhibited prolonged latency and interocular latency differences in the absence of clinical visual dysfunction. Median and tibial nerve evoked cortical potentials were severely attenuated in the absence of somatosensory deficit or peripheral nerve slowing. The far-field somatosensory potentials, however, were well preserved. All components of the auditory brain-stem potentials had latencies within normal limits. In the other, more severely afflicted, patient, all visual, somatosensory, and auditory evoked potentials were abnormal.     

Somatosensory evoked potentials in progressive supranuclear palsy

We report median and digital nerve somatosensory evoked potentials (SEPs) in 14 patients with probable progressive supranuclear palsy (PSP) along with transcortical long-loop reflexes, motor evoked potentials, and auditory startle responses. Enlarged cortical responses were found in 14 median and 13 digital nerve SEP studies, while long-loop reflexes were increased in only one patient. All motor evoked potential studies were normal. Auditory startle responses were either absent or reduced in 11 patients. The observed neurophysiological abnormalities may reflect cortical hyperexcitability but are distinct from those in other disorders associated with giant SEPs, such as progressive myoclonus epilepsy. A number of groups reported widespread cortical changes in addition to the characteristic subcortical neurofibrillary degeneration in post-mortem confirmed PSP. However, clinical features reflecting cortical dysfunction such as ideomotor apraxia and cortical sensory loss are uncommon in classical PSP. Furthermore, frontal lobe dementia which is frequently present in PSP patients, is thought to be of subcortical origin resulting from striato-frontal deafferentation. We propose that cortical neurofibrillary pathology may lead to subclinical intracortical disinhibition accounting for the enlarged cortical SEPs in PSP.     

Prognostic value of early cortical somatosensory evoked potentials after resuscitation from cardiac arrest

Short-latency somatosensory evoked potentials (SEPs) were evaluated in patients after cardiorespiratory arrest to study their pattern of recovery in the acute stage of anoxic-ischaemic coma. Fifty consecutive comatose patients were investigated within 8 h after cardiorespiratory resuscitation. In 30 patients no cortical SEPs were recorded and none of the patients recovered cognition. In 20 patients cortical SEPs were recorded and 5 recovered. The different susceptibility of frontal and parietal cortical structures to anoxia was reflected by the dissociated loss of parietal or frontal potentials in 6 patients. Post-mortem pathology in 15 patients confirmed extensive anoxic-ischaemic damage of cerebral and cerebellar cortex and thalamus in patients without cortical SEPs whereas the histological lesions were restricted to Sommer's sector and Purkinje cells in those with preserved SEPs. SEPs thus reflect the extent of brain damage after cardiorespiratory resuscitation.     

Motor and somatosensory evoked potentials in asymptomatic spondylotic cord compression.

To assess whether electrophysiological tests are of use in differentiating between patients with asymptomatic cervical stenosis and patients with clinical evidence of myelopathy, we studied motor evoked potentials (MEPs) to magnetic brain stimulation and somatosensory evoked potentials (SEPs) in patients with asymptomatic cervical cord compression and compared the results to healthy age-matched controls. The MEPs were normal in 23 of 25 patients and SEPs in 22 of 23 patients. Thus, MEPs and SEPs are normal in most cases of asymptomatic cervical stenosis. As previous studies have shown MEPs, and to a lesser extent SEPs, to be sensitive in the detection of spondylotic myelopathy, our data indicate that MEP and SEP may be clinically useful for differentiating patients with cervical stenosis who have myelopathy from those who have not.     

Dissociation of somatosensory and motor evoked potentials in non-comatose patients after head injury.

OBJECTIVES: This study was performed to evaluate the clinical value of combined use of somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) in patients with different brain lesions after head trauma. METHODS: A total of 64 patients with minor and moderate head injury were investigated by means of SEPs recorded over the parietal and frontal areas and MEPs following single-pulse transcranial magnetic stimulation (sTMS) and slow-rate repetitive transcranial magnetic stimulation (rTMS). RESULTS: In almost 50% of the patients, a dissociated impairment of somatosensory and motor evoked potentials was found. This dissociation was related to different distribution of SEP and MEP abnormalities in head injury subgroups. The higher threshold to sTMS and increased variability of the MEP amplitude during slow-rate rTMS were the most prominent features in patients with focal brain contusions, suggesting impairment of the cortical excitability. SEP abnormalities, as well as central conduction impairments, were more noticeable in patients with diffuse brain injury. CONCLUSIONS: A combined analysis of SEPs and MEPs may improve the assessment of cortical dysfunctions and central conduction abnormalities in non-comatose patients with head injury. A slow-rate rTMS may be considered as a complementary technique to the evaluation of the threshold in assessment of the excitability of the motor cortex in minor and moderate head injury.     

Time course of frontal somatosensory evoked potentials. Relation to L-dopa plasma levels and motor performance in PD.

OBJECTIVE: To verify whether the change in L-dopa plasma levels after a single dose of carbidopa/L-dopa 50/200 (controlled-release) transiently modifies frontal components of somatosensory evoked potentials (SEPs) in patients with PD in parallel with improvement of motor performance. BACKGROUND: Apomorphine, a potent dopamine-agonist drug, transiently increases frontal SEP components, which may be depressed in PD; however, relationships between clinical status, frontal SEPs, and therapy are still unclear. METHODS: Nineteen PD patients (mean age 65.9 years, range 52 to 77, responders to L-dopa therapy, were studied in the same day at times T0 (baseline predose level), T1 (presumed L-dopa peak time), and T2 (end of dose-induced motor response). The following were monitored: L-dopa plasma concentration, tapping test, reaction times, peak latency (with central conduction times), and amplitude of cervical, subcortical, as well as cortical parietal and frontal SEP components elicited by median nerve stimulation of the more clinically affected arm. RESULTS: The average amplitude of frontal components of PD patients was significantly reduced at T0 with respect to control subjects. A significant and transient amplitude increase of frontal SEPs was found at T1, in parallel with the L-dopa peak concentration and improvement in motor performance (tapping and reaction times), without significant changes in amplitude of parietal SEP waves. No latency shifts were observed in brain and spinal waves. CONCLUSIONS: L-Dopa may influence the responsiveness of the parkinsonian brain as assessed by frontal somatosensory evoked potentials. The time course of these modifications coincides with that of the clinical response in the motor performance.     

The prognostic value of evoked responses from primary somatosensory and auditory cortex in comatose patients.

OBJECTIVE: To evaluate somatosensory and auditory primary cortices using somatosensory evoked potentials (SEPs) and middle latency auditory evoked potentials (MLAEPs) in the prognosis of return to consciousness in comatose patients. METHODS: SEPs and MLAEPs were recorded in 131 severe comatose patients. Latencies and amplitudes were measured. Coma had been caused by transient cardiac arrest (n=49), traumatic brain injury (n=22), stroke (n=45), complications of neurosurgery (n=12) and encephalitis (n=3). One month after the onset of coma patients were classified as awake, still comatose or dead. Three months after (M3), they were classified into one of the 5 categories of the Glasgow outcome scale (GOS). RESULTS: At M3, 41.2% were dead, 47.3% were conscious (GOS 3-5) and 11.5% had not recovered consciousness. None of the patients in whom somatosensory N20 and auditory Pa were absent did return to consciousness and in the post-anoxic group, reduced cortical amplitude too was always associated with bad outcome. Conversely, N20 and Pa were present, respectively, in 33/69 and 34/69 patients who did not recover. CONCLUSIONS: The prognostic value of SEPs and MLAEPs in comatose patients depends on the cause of coma. Measurement of response amplitudes is informative. Abolition of cortical SEPs and/or cortical MLAEPs precludes post-anoxic comatose patients from returning to consciousness (100% specificity). In any case, the presence of short latency cortical somatosensory or auditory components is not a guarantee for return to consciousness. Late components should then be recorded.     

Lazarus' sign and respiratory-like movement in a patient with brain death

In the diagnosis of brain death, it is generally accepted that respiratory function has to be absent, however, spinal reflexes can be preserved. We presented a patient who showed a complex movements of upper limbs (Lazarus' sign) and respiratory like movement during the apnea test for the determination of brain death. This 72-year old female admitted to our hospital in a semicomatous state due to severe subarachnoid and ventricular hemorrhage. Her conscious level suddenly deteriorated to deep coma because of second hemorrhage on the same day. She became apnea and no brain stem reflexes elicited. Three days later, electrophysiological examination revealed a flat recording of electroencephalography, absence of auditory evoked potentials and no response of blink reflex. Short latency somatosensory evoked potentials obtained by median nerve stimulation showed the presence of Erb's N9 and spinal N13-P 13 components originating from cervical dorsal horn, however, the scalp P13 generated by cervico-medullary junction was absent. This patient fulfilled all other criteria for brain death. Four days after, an apnea test was performed. Spontaneous movements of both upper limbs were observed starting between 7 and 8 minutes after disconnecting the intubation tube from the ventilator. Both arms flexed at the elbow, abducted and elevated from the bed. Then, both hands were brought up to chest. Wrist and fingers were in a neutral position (Lazarus' sign). Simultaneously, shallow and irregular respiration like movements were recognized. These movements ceased immediately after connecting the respirator. These two types of movements were reproducible except for in the final test. Blood pressure gradually decreased, and cardiac arrest occurred one hour after.(ABSTRACT TRUNCATED AT 250 WORDS)     

Inadequacy of the forehead reference montage for detecting abnormalities of the spinal N13 SEP in cervical cord lesions.

Cervical somatosensory evoked potentials (SEPs) recorded using forehead and anterior cervical reference montages were compared in 6 patients whose MRI showed a cervical syrinx. All patients presented with a segmental loss of pain and temperature sensation in upper limbs, but no clinical evidence of dorsal column system dysfunction. Cervical SEPs recorded using the forehead reference montage were normal in all cases, while the N13 potential recorded using an anterior cervical reference was reduced, or absent, in 11 median nerve SEPs out of 12. This discrepancy results from persisting scalp P13-P14 far-field potentials, which were picked up by the forehead, but not by the anterior cervical, reference. It is concluded that the forehead reference montage is inadequate for assessing selectively the spinal N13 potential and should be abandoned for cervical SEP recording.