Moderate Neurological Deficit Research Articles

SUDDEN CARDIOCIRCULATORY COLLAPSE AND PRIMARY BRAIN TUMOR – A CASE REPORT AND A REVIEW OF THE LITERATURE

Background. We are presenting a case of 62-year old woman with acute cardiocirculatory collapse with signs of obstructive shock. Methods. After succesfull cardiopulmonary resuscitation (CPR) massive pulmonary thrombembolism was excluded by helical chest CT, but following brain CT revealed a brain tumor surrounded by abundant brain edema. With regard to all the accomplished diagnostic procedures, clinical picture, further clinical course and response to treatment, neurogenic cause of obstructive shock was most probable. Results. After surgical removal of glioblastoma, the patient was discharged from the hospital with moderate neurological deficit. Conclusions. During the course of brain tumors acute cardiocirculatory failure presented as a obstructive shock can evolve, because of local effects on brain circulatory (vasomotor) centers.

Long-Term Outcomes of Pediatric Moyamoya Disease Treated by Encephalo-Duro-Arterio-Synangiosis

To investigate the efficacy of encephalo-duro-arterio-synangiosis (EDAS) for the treatment of pediatric moyamoya disease, we analyzed 11 patients who were followed up for more than 100 months. Among 22 sides in 11 patients, we performed EDAS on 16 sides in 10 pa- tients, encephalo-duro-arterio-myo-synangiosis (EDAMS) on 5 sides in 4 patients and encephalo-myo-synangiosis (EMS) on 1 side. Of the 11 patients, 8 patients showed normal development and had no neurological deficit. The remaining 3 patients showed mild to moderate neurological deficits, but in these cases, pre- and perioperative insults were considered to be attributable to the morbidities. Of 13 sides treated by EDAS, well-developed neovascularization was observed in 12. However, well-developed neovascularization was observed in only 3 out of 6 sides treated by EMS or EDAMS. These data might indicate that EDAS is a therapeutic alternative for the surgical treatment of pediatric moyamoya disease.

Neurological Outcome in Comatose Children with Bilateral Loss of Cortical Somatosensory Evoked Potentials

Bilateral loss of median nerve cortical somatosensory evoked potentials (SEP) in comatose patients is reported to be one of the most discriminating predictors of poor outcome. We reviewed 53 children with bilateral absent cortical SEP with respect to their outcome and their follow-up SEP. Brain injury was caused by global cerebral ischaemia in 18 children, severe head trauma (SHT) in 13, nervous system infections in 10, and other aetiologies in 12 children. Thirty of 53 children died within the first 4 weeks and another 8 children within 4 years after the event. Two children (both ischaemia) survived in a persistent vegetative state, 9 children (1 ischaemia, 2 SHT, 3 nervous system infections, 3 other aetiologies) survived with severe deficits and 4 children (all SHT) with mild or moderate deficits. In 30 children SEP were repeated and in 8 children (5 SHT, 2 nervous system infection, 1 other aetiology) unilateral or bilateral cortical responses reappeared. Although bilateral loss of cortical SEP predicted an unfavourable outcome in most patients, a few comatose children with SHT showed an outcome with mild or moderate neurological deficits.

Factors correlated with hypermetabolism in patients with amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is a severe disease characterized by neurogenic amyotrophy and degeneration of upper and lower motor neurons. Although ALS patients usually experience reductions in fat-free mass (FFM), hypermetabolism via an undetermined source has also been reported. The objective was to clarify the metabolic level of ALS patients. We measured the resting energy expenditure (REE) of 62 patients (32 men and 30 women) with ALS and investigated the factors correlated with metabolic level. Nutritional evaluation included bioelectrical impedance analysis, indirect calorimetry, and calculation of the body mass index. Neurologic assessment included an evaluation of peripheral and central neurologic deficit. Forced vital capacity was measured and smoking status was noted. A complete blood cell count was made and thyroid hormone and C-reactive protein concentrations were measured. Patients were hypermetabolic, by an average of approximately 10% more than in a reference healthy population. FFM, age, and the neutrophil count were significantly associated with REE. The only variable that contributed to the prediction of REE, REE/Z100 kHz (bioimpedance at 100 kHz), REE adjusted for FFM, or the ratio of measured REE to calculated REE was the neutrophil count, which explained only a small percentage of variance in the multiple regression analysis. Hypermetabolism was not associated with a reduction in respiratory function, tobacco use, hyperthyroidism, spasticity and fasciculation intensities, or infection. Our study corroborates the surprising finding that ALS patients are hypermetabolic. FFM, age, sex, manual muscular testing, the modified Norris limb score, weight, and an increase in circulating neutrophil counts correlated with the hypermetabolic state. Other factors may play a role in pathophysiologic processes that involve mitochondrial energy production or even sympathoadrenergic activation.

Iodine deficiency disorders in Europe.

Iodine deficiency disorders (IDD) are related to the degree of iodine deficiency. In European countries, characterized by mild to moderate iodine deficiency, neurological deficits or minor neuropsychological impairments have been described. Urinary iodine excretion (UIE) ranged from 30 to 170 mcg/L, 141 millions of people were at risk of IDD, 97 millions were affected by goiter and 0.9 millions had an impaired mental development. Iodine prophylaxis is devoid of adverse reactions with the exception of sporadic cases of transitory hyperthyroidism, associated to the severity of iodine deficiency before the prophylaxis. The International Council for Control of IDD recommends an universal iodine prophylaxis, instituted gradually in severe iodine deficient countries. The total cost of universal iodine prophylaxis is very cheap compared to the social cost of goiter and cretinism. In conclusion, most European countries are still characterized by mild to moderate iodine deficiency. Iodine prophylaxis programs are already operating, its cost is irrelevant with respect to the undebatable beneficial impact on the health. Adverse effects are not observed except in severe iodine deficient areas where iodine intake was abruptly increased.

Characterization of mouse brain-specific angiogenesis inhibitor 1 (BAI1) and phytanoyl-CoA alpha-hydroxylase-associated protein 1, a novel BAI1-binding protein

Previously, PAHX-AP1 (PAHX-associated protein 1) was isolated as a novel protein to interact with Refsum disease gene product (phytanoyl-CoA alpha-hydroxylase, PAHX) and specifically expressed in mouse brain. PAHX-AP1 is also suggested to be involved in the development of the central neurologic deficits of Refsum disease. To clarify its function, we have searched for proteins that associate with PAHX-AP1 via yeast two-hybrid system. We found that PAHX-AP1 interacts with the cytoplasmic region of human brain-specific angiogenesis inhibitor 1 (hBAI1), and isolated murine homolog of hBAI1. Structural analysis of the PAHX-AP1 with three reported hBAI-associated proteins (BAP) revealed no homology among them, and we designated PAHX-AP1 as BAP4. The ability of BAP4 to interact with BAI1 was confirmed by pulling-down BAI1 with GST-BAP4 protein and immunoprecipitation study using brain lysate. Northern and Western blot analyses demonstrated a unique pattern of BAI1 expression in the brain. The peak level of BAI1 was observed 10 days after birth. In situ hybridization analyses of the brain showed the same localization of BAI1 as BAP4, such as most neurons of cerebral cortex, hippocampus, and V, VI, VII, VIII, and XII nuclei. Because BAI1 possessed thrombospondin-type 1 repeats in its extracellular region, changes of BAI1 expression were examined in the focal cerebral ischemia model. The BAI1 expression decreased on the ischemic side after 24 h but BAP4 was not changed after the time-course of ischemia. Our results indicate that expression and localization of BAI1 in the brain is correlated with BAP4, and that BAI1 is involved in inhibition of angiogenesis and neuronal differentiation.

Intravenous Administration of Magnesium Sulfate in Acute Stroke: A Randomized Double-blind Study

A randomized, placebo-controlled, double-blind study was performed as a pilot study to examine the benefit of the administration of magnesium sulfate given intravenously as a protective substance during the first 24 hours following a stroke. Patients who had cortical infarction in the middle cerebral artery territory with moderate to severe neurologic deficits lasting for more than 15 minutes with onset less than 24 hours were included. The patients were treated with magnesium sulfate or placebo for 5 days and examined by a blinded investigator. Patients had follow-up for 30 days. The primary efficacy variable was the proportion of patients reaching mild to moderate neurologic deficit on the Orgogozo scale (80 points) and relative functional independence on the Barthel index (60 points). Orgogozo scale and Mathew scale values were obtained on admission and days 2, 4, 8, and 30 after stroke. Barthel activities of daily living index and Rankin disability score were obtained on day 30. Forty-one patients (22 given treatment and 19 given placebo) demonstrated significant beneficial effects on the Orgogozo scale (84 +/- 11 vs. 64 +/- 10, p < 0.0001) and (83 +/- 14 vs. 70 +/- 15, p < 0.009), respectively. At the end of 1-month follow-up, the Barthel ADL index was nonsignificantly higher and the Rankin disability score was marginally significantly lower in the magnesium-treated group (84 +/- 26 vs. 71.8 +/- 26, p < 0.143) than in control subjects (2.3 +/- 1.1 vs. 3 +/- 1.3, p < 0.077). Intravenous magnesium sulfate had significant positive effect on the outcome in patients with acute stroke. Further studies on a larger scale are needed to confirm these findings.

Predictors of resource use after acute hospitalization: the Northern Manhattan Stroke Study.

To determine demographic and clinical predictors of discharge destinations following acute care hospitalization for stroke in the community of northern Manhattan. A group of 893 patients (mean age, 70 +/- 12 years; 56% women; 51% Hispanic, 30% African-American, 19% white) who survived acute care hospitalization for a first ischemic stroke were followed prospectively. Stroke severity was assessed by the NIH Stroke Scale and categorized as mild (< or = 5), moderate (6 to 13), and severe (> or = 14). Polytomous logistic regression was used to determine predictors for rehabilitation and nursing home placement versus returning home. Among the survivors of acute stroke care hospitalization, 611 (68%) patients were discharged to their homes, 168 (19%) to rehabilitation, and 114 (13%) to nursing homes. Patients with moderate and severe neurologic deficits had more than a threefold increased risk of being sent to a nursing home and more than an eightfold increased risk of being sent to rehabilitation. Age over 65 and cognitive impairment were associated with placement to a nursing home (age over 65: OR, 2.4; 95% CI, 1.0 to 5.6; cognitive impairment: OR, 2.9; 95%, CI 1.4 to 5.7), and rehabilitation (age over 65: OR, 1.8; 95% CI, 1.1 to 2.9; cognitive impairment: OR, 2.9; 95% CI, 1.4 to 5.7). Our results demonstrated that one-third of patients with acute stroke from the community of northern Manhattan required placement in a temporary or a long-term disability care institution following acute care hospitalization. Severity of stroke is an important factor that influences discharge planning following acute care hospitalization and its reduction can improve health care resource usage.

Continued experience with physical examination alone for evaluation and management of penetrating zone 2 neck injuries: Results of 145 cases

Purpose: Our preliminary experience with physical examination alone in the evaluation of penetrating zone 2 neck injuries for vascular trauma was previously reported in 28 patients over a 2-year period (1991-1993). The purpose of the current study was to examine the results of this approach in a much larger group of patients over an 8-year period. Methods: The medical records for all patients admitted to our level I trauma center (all of them entered into our prospective protocol) between December 1991 and April 1999 with penetrating zone 2 neck trauma were reviewed for their initial presentation and any documented vascular injury. Results: A total of 145 patients made up the study group; in 30 of these patients, the penetrating trajectory also traversed zone 1 or 3. Thirty-one patients (21%) had hard signs of vascular injury (active bleeding, expanding hematoma, bruit/thrill, pulse deficit, central neurologic deficit) and were taken immediately to the operating room; 28 (90%) of these 30 patients had either major arterial or venous injuries requiring operative repair (the false-positive rate for physical examination thus being 10%). Of the 114 patients with no hard signs, 23 underwent arteriography because of proximity of the injury to the vertebral arteries or because the trajectory included another zone. Of these 23 arteriograms, three showed abnormalities, but only one required operative repair. This case had no complications relating to the initial delay. The remaining 91 patients with no hard signs were observed without imaging or surgery for a minimum of 23 hours, and none had any evidence of vascular injury during hospitalization or during the initial 2-week follow-up period (1/114; false-negative rate for physical examination, 0.9%). Conclusions: This series confirms the earlier report indicating that patients with zone 2 penetrating neck wounds can be safely and accurately evaluated by physical examination alone to confirm or exclude vascular injury. The missed-injury rate is 0.7% (1/145) with this approach, which is comparable to arteriography in accuracy but less costly and noninvasive. Long-term follow-up is needed to confirm this management option. (J Vasc Surg 2000;32:483-9.)

Identification of a brain specific protein that associates with a Refsum disease gene product, phytanoyl-CoA alpha-hydroxylase

Refsum disease is an autosomal recessive neurologic disorder of the lipid metabolism. Major diagnostic clinical findings include retinitis pigmentosa, peripheral polyneuropathy, cerebellar ataxia, increased cerebrospinal fluid protein without pleocytosis, nerve deafness, and cardiac involvement. We have identified a novel protein (PAHX-AP #1) associated with phytanoyl-CoA alpha-hydroxylase (PAHX), a Refsum disease gene product, using the yeast-based two-hybrid assay. The middle portion (amino acids 83–264) of PAHX was used as a bait and a mouse brain cDNA library was searched. The ability of PAHX-AP #1 to interact with PAHX was confirmed using immunoprecipitation and Western blot studies in NIH3T3 cells which stably expressed both PAHX and PAHX-AP #1. Northern and Western blot analyses demonstrated a unique pattern of developmental PAHX-AP #1 expression which was targeted to the adult brain, but ubiquitous expressions of PAHX were observed in all examined tissues. In situ hybridization analyses of the brain showed specific localization of PAHX-AP #1 to the supragranular layer in the cerebral cortex, dentate gyrus, hippocampus, Purkinje cell layer, deep cerebellar nucleus, trigeminal nucleus, abducent nucleus, facial nucleus, cochlear and vestibular nucleus, ganglion cell and nuclear layer of the retina. These data indicate that localization of PAHX-AP #1 in the brain is correlated with central neurologic symptoms of Refsum disease such as retinitis pigmentosa, cerebellar ataxia, nerve deafness and suggest that PAHX-AP #1 may be involved in the development of the central neurologic deficits of Refsum disease.

Self-assessment questions

A 16-year-old Indian girl has been in the UK for 3 months and is due to take part in an arranged marriage. A week before, she saw her GP for nausea in the mornings. He prescribed Iron as she was pale, but ordered no investigations. She presents to A&E 6 hours after ingesting 20 x 200 mg of Ferrous Sulphate. Her fiancee acts as interpreter and says she had forgotten to take some tablets and then attempted to catch up in one go. Her past medical history was unremarkable and there was no significant family history. She ate a balanced diet and her weight was stable, normal periods, no melena and no other medication. On examination she was pale and vomiting. Cardiorespiratory systems stable, mildly tender abdomen but no hepatosplenomegaly. No central or peripheral neurological deficit. Hb 10.1 g/dl, MCV 62 fl, MCH 20 pg, PLT 237 10 9/l, WCC 11 10 9/l. B12, folate & ferritin within normal limits.

Superselective Intra-Arterial Thrombolysis for Acute Cardioembolic Stroke in a Child with Idiopathic Dilated Cardiomyopathy

We describe a case of cardioembolic dominant hemisphere internal carotid artery occlusion in a child with idiopathic dilated cardiomyopathy. The patient was subjected to superselective local intra-arterial thrombolysis using recombinant tissue plasminogen activator (A lteplase; Actilyse((R))). In presence of good collateral flow local intra-arterial thrombolysis prevented a major dominant hemisphere ischaemic stroke, although post-interventional computed tomographic scans disclosed haemorrhagic conversion in the left corpus striatum. Forty eight months after ischaemic stroke and thrombolysis the patient is ambulatory with a moderate neurologic deficit.

Efficacy of intraarterial thrombolysis of basilar artery stroke

Stroke from basilar artery (BA) occlusion is a devastating neurological event with reported mortality rates of up to 90%. This series reports our experience in 15 cases using intraarterial (IA) thrombolysis to treat basilar artery stroke at the Oregon Stroke Center. Over a 4-year period, consecutive cases of basilar artery stroke were treated with IA urokinase (UK) if they met the following criteria: had a baseline National Institutes of Health Stroke Scale (NIHSS) score greater than 6; symptoms began within 48 hours; had no or minimal early infarct signs on computed tomography (CT) scan; and angiogram confirmed basilar occlusion. Patients were treated with UK infused via a microcatheter directly into the clot. Angiographic efficacy was assessed by a repeat angiogram at the end of infusion and clinical efficacy was determined by NIHSS evaluation at 48 hours and 3 months. Fifteen patients, mean age 59 (16 to 78) and baseline NIHSS of 30 (7 to 40), were treated at a mean of 12 hours (4 to 48). An average dose of 500,000 (150,000 to 1,250,000) units of UK was given over 1 to 2 hours. Excellent vessel recanalization occurred in 12 of 15 (80%) patients. All three cases without recanalization died within 48 hours (100%). Of the 12 patients with recanalization, 2 died (16.7%), whereas the 9 of 10 remaining had mild or moderate neurological deficits (mean NIHSS of 5) at 3 months. IA thrombolysis has the potential to decrease mortality and improve outcome in cases with severe basilar artery stroke even when administered after 6 hours.

Extracorporeal membrane oxygenation for nonneonatal pulmonary and multiple-organ failure

Purpose: Extracorporeal membrane oxygenation (ECMO) is an accepted therapy for neonatal pulmonary failure, but its use in older children has been controversial. Methods: Over 13 years, 55 children (ages, 3 months to 16 years) were treated with venoarterial or venovenous ECMO. The diagnoses were viral, bacterial, or fungal pneumonia (24 patients); hydrocarbon or gastric aspiration (n = 10); adult respiratory distress syndrome (ARDS), sepsis, near drowning (n = 15); pulmonary contusion (n = 2); airway obstruction (n = 3); pulmonary artery foreign body (n = 1). Pre-ECMO blood gas ranges (and means) were Po 2, 21 to 100 (n = 44); Pco 2, 23 to 125 (n = 72); pH, 6.81 to 7.55 (n = 7.11). Results: All patients received inotropes, and 38 required dialysis or hemofiltration. ECMO was used for 20 to 613 hours (mean, 196 hours). Patient complications included cannulation site hemorrhage (n = 40), renal failure (n = 10), seizures (n = 8), stroke (n = 3), and cerebral hemorrhage (n = 2). Twenty-five patients (45%) survived ECMO, with 21 long-term survivors (10 pneumonia, five aspiration, five ARDS, one pulmonary contusion), five of whom have mild to moderate neurological deficit. Patients with combinations of pulmonary, cardiac, and renal failure, or sepsis did not survive. Conclusions: ECMO is an invasive technique that can be life saving in the child with isolated respiratory failure, but its usefulness in children with multiorgan failure is less certain.

Spinal cord GLT-1 glutamate transporter and blood glutamic acid alterations in motor neuron degeneration (Mnd) mice

This study characterizes for the first time neurochemical mechanisms in Mnd mice, initially described as a model of motor neuron disease and more recently proposed as a model for neuronal ceroid lipofuscinosis. A selective decrease (−30%) of [ 3H]glutamate uptake was found in spinal cord but not cortical synaptosomes of Mnd mice aged 28 weeks, when they show histopathological alterations, complete blindness and moderate neurological deficits. In spite of the widespread presence of stored material in neurons in many brain regions and spinal cord, the active transport of [ 3H]serotonin, [ 3H]dopamine and depolarization-induced [ 3H]serotonin release were not affected. Spinal EAAC1 glutamate transporter protein was significantly decreased in some but not all aged mice by 36% on average, possibly due to the loss of motor neurons. GLT-1 immunoreactivity was reduced by 34% in 28-week-old Mnd mice, while GLAST immunoreactivity was not affected. In Mnd mice aged 14 weeks, when there was no apparent alteration of motor function, the defect in the glial transporter protein GLT-1 was similar to that in 28-week-old mice (25%). Blood glutamic acid concentration was increased in Mnd mice aged 14–22 weeks. We suggest that the early decrease of GLT-1 protein might raise the extrasynaptic glutamic acid concentration, and contribute to the loss of motor neurons in affected mice, resulting in low [ 3H]glutamate uptake, low EAAC1 immunoreactivity and neurological deficits.

The forgotten condyle: Delayed hypoglossal nerve palsy caused by fracture of the occipital condyle

Fracture of the occipital condyle is a rare injury that can be easily overlooked. Palsies of lower cranial nerves can be the only symptom of the fracture. We report a patient with isolated post-traumatic hypoglossal nerve palsy who developed hypoglossal nerve palsy within 2 months after a car accident, indicating that the acute trauma itself did not damage the hypoglossal nerve. Most likely the palsy is caused by pressure to the nerve prior to the entry or within the hypoglossal canal. Since, in the present case, the fracture was stable and the patient showed only moderate neurological deficits, the operation was deferred.

Diagnosis and management of blunt carotid artery injury in oral and maxillofacial surgery

Purpose: Traumatic occlusion of the internal carotid artery (ICA) is a rare complication of maxillofacial trauma or surgery. This investigation evaluated patient demographics, diagnostic methods, and effective therapeutic modalities associated with blunt carotid injury (BCI). Patients and Methods: This was a retrospective analysis of patient records with an ICD-9-CM diagnosis of carotid injury conducted at MetroHealth Medical Center during the 24-month period between August 1993 and July 1995. Carotid injuries attributable to penetrating trauma were excluded. Age, gender, cause of injury, Glasgow Coma Scale score, Injury Severity Score, type and location of injury, concomitant injury, diagnostic methods, treatment modalities, and outcome were identified, recorded, and analyzed. Results: During the 24-month period, 12 patients (seven males and five females) suffered BCI. These patients were divided into two groups based on cause of the problem. In group I, there were 3,214 blunt trauma patients admitted during the 2-year study, of which 10 patients had BCI, representing 0.31% of blunt trauma patients, and 1.2% of patients with head injuries. Seven patients presented with hemiplegia, two with cranial nerve palsy, and one with perceptual neglect. Ninety percent of the patients had associated injuries. Two patients had surgical intervention, three received anticoagulation, and five had only supportive care. Four of the 10 patients died, four had moderate neurologic deficits, and two survived with only minor neurologic deficits. In group II, two patients developed BCI after surgery. A 52-year-old woman had a carotid injury after right total temporomandibular joint replacement, and a 48-year-old man who underwent surgical removal of a third molar became hemiplegic postoperatively. The first patient recovered after anticoagulation, whereas the second patient, who received only supportive care, has severe neurologic deficits. Conclusions: BCI is an uncommon entity. It is usually recognized when a patient develops an unexplained neurologic deficit, most often hemiplegia, subsequent to trauma or surgery of the head, face, or neck. In the early stages, the diagnosis can be missed by carotid ultrasound or computed tomography. The injury is unrelated to Glasgow Coma Scale score. Symptoms may not develop for days after injury in 50% of patients. Anticoagulation appears to be the most beneficial therapeutic modality.

Surgical Aspects of Fusiform and Saccular Extracranial Carotid Artery Aneurysms

The purpose of this paper is to analyse surgical aspects of aneurysms of the distal extracranial internal carotid artery. Nine cases of extracranial carotid artery aneurysm are reported. Five were fusiform, located at the carotid bifurcation, and four were saccular, confined to the internal carotid artery. An end-to-end plication technique and Dacron patch angioplasty were employed for all fusiform aneurysms. In three saccular lesions, resection and 4-mm polytetrafluoroethylene (PTFE) graft interposition were carried out. In one case with a high lesion, ligation of the carotid artery was performed. Ligation resulted in severe postoperative stroke and fatal outcome. One patient with a saccular lesion developed a transient ischaemic attack after the operation. In other patients no central neurological deficit was produced by the surgery itself. Transient cranial nerve damage occurred in four patients (two hypoglossal nerve; two superior laryngeal nerve). As demonstrated by these cases, synthetic material may be used in restoration of the carotid artery. It is concluded that, according to type, location of the aneurysm and adequacy of contralateral cerebral blood flow, selective management is necessary.

Surgical aspects of fusiform and saccular extracranial carotid artery aneurysms

The purpose of this paper is to analyse surgical aspects of aneurysms of the distal extracranial internal carotid artery. Nine cases of extracranial carotid artery aneurysm are reported. Five were fusiform, located at the carotid bifurcation, and four were saccular, confined to the internal carotid artery. An end-to-end plication technique and Dacron patch angioplasty were employed for all fusiform aneurysms. In three saccular lesions, resection and 4-mm polytetrafluoroethylene (PTFE) graft interposition were carried out. In one case with a high lesion, ligation of the carotid artery was performed. Ligation resulted in severe postoperative stroke and fatal outcome. One patient with a saccular lesion developed a transient ischaemic attack after the operation. In other patients no central neurological deficit was produced by the surgery itself. Transient cranial nerve damage occurred in four patients (two hypoglossal nerve; two superior laryngeal nerve). As demonstrated by these cases, synthetic material may be used in restoration of the carotid artery. It is concluded that, according to type, location of the aneurysm and adequacy of contralateral cerebral blood flow, selective management is necessary. © 1997 The International Society for Cardiovascular Surgery.

How reliable is the predictive value of SEP (somatosensory evoked potentials) patterns in severe brain damage with special regard to the bilateral loss of cortical responses?

In patients sustaining severe brain damage (SBD), prediction of later outcome is often very difficult, in particular under conditions of therapeutic management like relaxation and intravenous phenobarbital. Somatosensory evoked potentials (SEP) correlated best with later prognosis and expected neurological deficit. In detail, the primary bilateral loss of cortical responses (BLCR) is regarded to be a reliable marker for poor prognosis. The goal of the following prospective study was to reassess the prognostic value of early serial median nerve SEP recording in severe brain damage in comparison to other neurophysiological, clinical, and neuroradiological parameters and, additionally, to test the hypothesis, that the BLCR-pattern is always associated with a poor prognosis and is never reversible. Prospective study. Anaesthesiological hospital intensive care unit. 42 comatose patients with severe brain damage (29 males/13 females), mean age 39.6 +/- 19.3 years, mean initial Glasgow Coma Score (GCS) 6.6 +/- 3.1, investigated by means of median somatosensory evoked potentials (SEP) and brainstem auditory evoked potentials (BAEP) with serial recordings on day 1, 3 to 4, and 8 to 1, and repeated cranial computerized tomography. We classified the outcome according to the Glasgow Outcome Scale (GOS). Our data showed a high correlation of initial SEP scores (Spearman correlation coefficient = -0.70) with outcome for both a favorable and an unfavorable prognosis (p = 0.0001). The reliability increased with serial recordings. The SEPs showed superiority to parallel brainstem auditory evoked potentials (Spearman correlation coefficient = -0.50, p = 0.0007), GCS, and standardized neuroradiological criteria. Primary (BLCR) occurred in 16 patients (38%) and implied a fatal prognosis in all adult patients (n = 15, specificity = 93.3%, sensitivity = 59.3%). In contrast, a young child with predominant brainstem hemorrhagic contusions regained consciousness and developed mild to moderate neurological deficit (GOS 3-4) during long-term follow-up of 4 years. This clinical improvement paralleled bilateral asymmetric recovery of cortical SEP responses. SEP allow an early reliable assessment of both poor and good prognosis in SBD, in particular when applied serially. BLCR does not always imply a fatal diagnosis, as a circumscribed contusional lesion rarely may lead to selective reversible blockage of ascending somatosensory pathways in the brainstem. In contradiction to this lesional etiology, a hypoxia-induced BLCR pattern seems to correlate strictly with a poor prognosis, reflecting a different pathogenesis with diffuse destruction of cortex and thalamocortical pathways.