Short-latency somatosensory evoked potentials correlate with the severity of the neurological deficit and sensory abnormalities following cerebral ischemia

Short-latency somatosensory evoked potentials (SSEPs) were studied in 49 patients who had suffered hemispheric or thalamic ischemia, including 6 patients with transient ischemic attacks (TIAs) and 3 patients with reversible ischemic neurological deficits (RINDs). SSEPs were abnormal in 30 patients (61%). SSEP abnormalities correlated with the presence of sensory deficit and the degree of neurological deficit. SSEPs were normal following TIA but were abnormal in 2 of 3 patients with RINDs. SSEPs were abnormal in some patients without sensory deficits suggesting that sensory pathways may be affected when clinically inapparent.     

Atypical cobalamin deficiency. Subtle biochemical evidence of deficiency is commonly demonstrable in patients without megaloblastic anemia and is often associated with protein-bound cobalamin malabsorption

We performed studies in 25 patients with low serum cobalamin levels who had few if any clinical or hematologic findings of cobalamin deficiency. All but three had morphologically normoblastic hematopoiesis, and 15 were not even anemic. None of those tested excreted methylmalonic acid or homocystine. Nevertheless, the dUST identified metabolic abnormalities in 18 of the 25 cases. In vitro additives were essential in the dUST. Especially noteworthy was MTHF, whose addition unmasked an otherwise undetectable dUST abnormality in four cases. Why MTHF appears to act as a "stress test" in this setting is unknown but deserves further attention. Seven patients had early forms of classical malabsorptive states such as pernicious anemia, defined by abnormal Schilling test results. Among the rest, seven of 13 patients displayed malabsorption of protein-bound cobalamin despite normal absorption of free cobalamin by the Schilling test. In two patients, initially normal Schilling test results became abnormal the following year. These findings demonstrate that seemingly falsely low serum cobalamin levels often indicate subtle biochemical cobalamin deficiency. Early stages of pernicious anemia or other classical malabsorptive states are sometimes responsible for such subtle deficiency. However, malabsorption confined to protein-bound cobalamin is an equally common cause. Current concepts of cobalamin deficiency and the absorptive defects that can cause it should be expanded to include atypical defects requiring newer methods of identification.     

Assessment of median nerve somatosensory evoked potentials in cerebral ischemia

Seventy patients with cerebral ischemia (21 with transient ischemic attack and 49 with stroke) were studied with short-latency median nerve somatosensory evoked potentials to characterize the evoked potentials in all ischemic patients and to investigate their efficacy for prognosis in stroke. Within 72 hours of symptom onset, all 70 patients received a scaled neurologic function score, with a maximum of 50 points. Somatosensory evoked potential abnormalities were found in 10% (2/19), 42% (15/36), and 93% (14/15) of all patients with initial neurologic examinations who had normal (50 points), mild-moderate (30-49 points), and severe deficits (less than or equal to 29 points), respectively. Thirty-seven of the 49 stroke patients were available for a follow-up neurologic assessment. Eight-nine percent (8/9) of the stroke patients with poor outcome had somatosensory evoked potential abnormalities; 82% (9/11) of the stroke patients with severe neurologic deficits at onset had poor outcome. Results demonstrate that somatosensory evoked potential abnormalities are common in patients with cerebral ischemia but that somatosensory evoked potential findings are not significantly better than a detailed neurologic examination in predicting outcome from stroke.     

Triphasic waves: a reassessment of their significance

Electroencephalograms and case histories of 50 patients with triphasic waves were reviewed. EEGs were studied for slowed dominant activity, anteriorly dominant triphasic waves, anterior-posterior lag time and bursts of triphasic waves. Etiologies of triphasic waves were: hepatic (28), azotemia (10), anoxia (10) and hyperosmolarity (2). Sixteen hepatic and two azotemic patients showed all of these characteristic EEG features. Triphasic waves demonstrating all of these features are highly characteristic of but are not pathognomonic for hepatic encephalopathy. Prognosis correlated best with the type of hepatic injury and deteriorating renal function. We postulate that triphasic waves are generated by the same thalamocortical volleys which normally induce spindles.     

Short-latency somatosensory evoked potentials in myotonic dystrophy: evidence for a conduction disturbance

Short-latency somatosensory evoked potentials were recorded in 13 patients with myotonic dystrophy (MyD). The MyD were compared with age-matched controls. The mean conduction latency between the brachial plexus and dorsal column nuclei (EP-N14) was significantly longer for the MyD. Results suggest an afferent conduction disturbance in MyD.     

Suprasellar lesions: evaluation with MR imaging

The authors retrospectively evaluated the characteristics on magnetic resonance (MR) images of 59 suprasellar lesions and compared them with computed tomography (CT) scans in 55 of the cases in which CT was performed. A diverse number of lesions were included: 17 pituitary adenomas; eight optic or hypothalamic gliomas; six craniopharyngiomas; six vascular anomalies; four lesions with extension into the suprasellar space; three metastases; two each of meningioma, hamartoma, germinoma, sarcoid granuloma, and teratoma; and one each of lymphoma, optic tract hematoma, cerebrospinal fluid-borne metastasis, pituitary hyperplasia, and sphenoid sinus mucocele. MR enabled characterization of lesions containing hemorrhage, fat, flowing blood, mucus, and cyst and allowed more specific diagnoses than CT in 6% of cases. MR was equivalent to CT in allowing lesions to be detected and in 20% of cases more accurately defined altered perisellar anatomy. Vascular abnormalities can be better evaluated with MR, and use of angiography can be avoided in some cases.     

Unsuspected pernicious anemia in a patient with sickle cell disease receiving routine folate supplementation

Although the issue of folate supplementation in sickle cell anemia remains controversial, routine supplementation has become common. The major drawback to indiscriminate folate therapy is the potential of masking findings of vitamin B12 (cobalamin) deficiency. This has been dismissed as a problem in sickle cell anemia because of the generally young age of the patients. However, because young blacks, especially women, are at higher risk for developing pernicious anemia than whites, sickle cell anemia and pernicious anemia can be expected to coexist occasionally. In this article we describe such a patient and recommend that routine folate supplementation should not be given in sickle cell anemia before determining the vitamin B12 status.     

Neurologic and evoked potential abnormalities in subtle cobalamin deficiency states, including deficiency without anemia and with normal absorption of free cobalamin

The meaning of a low serum cobalamin level when the classic findings of pernicious anemia are lacking is undergoing reevaluation. We therefore studied the neurologic status of 11 patients who had low cobalamin levels without definite hematologic evidence of deficiency. Neurologic evaluation included pattern-shift visual and median and posterior tibial nerve somatosensory evoked potentials. None of the patients had megaloblastic changes in the blood or bone marrow, although 7 of the 11 had subtle cellular cobalamin disturbances demonstrated by an abnormal deoxyuridine suppression test result. Seven patients had normal Schilling test results and 2 had borderline results; however, 2 of the 5 patients tested further had food-cobalamin malabsorption, while a third had prepernicious anemia. The patients displayed a variety of neurologic problems, including dementia, depression, myelopathy, neuropathy, and seizure disorder; 1 patient was neurologically normal by clinical criteria. Evoked potential abnormalities were demonstrable in 8 of the 9 patients with subtle cobalamin deficiency, and in at least 5 cases the disturbance was central. In contrast, both patients whose low serum cobalamin levels were found on evaluation to be spurious had normal evoked potentials. Evoked potential abnormalities improved in the one patient retested after cobalamin therapy. These findings demonstrate that neurologic deficits occur not only in classic cobalamin deficiency but also in subtle or atypical cobalamin deficiency states in which anemia is absent and Schilling test results are normal. Electrophysiologic evidence of neurologic impairment is often present, even in patients without obvious clinical neurologic abnormalities.     

Comparison of MR and CT myelography in imaging the cervical and thoracic spine

MR imaging and CT myelography were compared in a retrospective study of 38 patients with suspected lesions of the cervical and thoracic spinal canal and cord. Twenty-eight abnormal cases were found, including spondylosis (9), tumors (8), intramedullary cavities (3), arachnoiditis (3), disk-space-centered infection or osteomyelitis (2), nonneoplastic cord swelling (2), and CSF-borne metastasis (1). MR was equal or superior to CT myelography in depicting cases of cord enlargement, cord compression, and cord atrophy, providing better tissue characterization, no shoulder artifact, and no limitation caused by CSF block. CT myelography was superior to MR in depicting cases of spondylosis and arachnoiditis. It showed superior spatial resolution, which was most pronounced when comparing axial images and hence particularly superior in detecting the lateral extent of disk herniation. Use of surface coils and thin imaging sections is essential for accurate and complete MR evaluation of the cervical and thoracic spine.     

Endograft repair of traumatic aortic transection in a 10-year-old--a case report

Blunt abdominal aortic injury from trauma is extremely rare. It is generally from motor vehicular crashes resulting in dissection, intramural hematoma, or free rupture. Timely recognition and treatment of this injury are essential for a chance for survival. To the authors knowledge, this is the first reported case of successful management of this injury, with use of an intravascular stent-graft, in a child. Although open aortic repair has been the only modality used in children, intravascular stent-graft can be another available option in these injuries.