Brian J. Anziska

Clinical Predictors of Abnormality Disclosed by Computed Tomography after Mild Head Trauma

We prospectively studied 712 consecutive patients during a 1-year period who presented with amnesia or loss of consciousness after nonpenetrating head trauma and who had a perfect Glasgow Coma Scale score of 15. Of the 67 (9.4%) patients with acute traumatic lesions disclosed by computed tomography (CT) of the head, 2 required neurosurgical intervention and 1 died. Four factors were statistically correlated (P < 0.05) with abnormal CT findings: Older age, white race, signs of basilar skull fracture, and being either a pedestrian hit by a motor vehicle or a victim of an assault. Sex, length of antero- or retrograde amnesia, forward and reverse digit spans, object recall, focal abnormality on the general neurological exam, and subjective complaints were not statistically correlated with CT abnormality. Using step-wise discriminant function analysis, no single item or combination of items could be used to classify 95% of the patients into either the normal or abnormal CT group. Therefore, regardless of age, mechanism of injury, or clinical findings, intracranial lesions cannot be completely excluded clinically on head-trauma patients who have loss of consciousness or amnesia, even if the Glasgow Coma Scale score is 15. However, only two patients (0.3%) required neurosurgical intervention.

Short latency somatosensory evoked potentials: Studies in patients with focal neurological disease

In non-cephalic reference recordings, the scalp recorded short latency evoked potentials to median nerve stimulation in normal subjects consist of 3 positive potentials followed by a negative potential. The sources of these potentials have not been precisely defined. Therefore, these potentials were recorded in 31 patients with focal lesions of the nervous system. Recordings were evaluated for (a) the presence or absence of these potentials and (b) peak latency differences between components. The results were compared with similar data obtained on 25 normal control subjects. Only the first positive potential was recorded with stimulation ipsilateral to the lesion in one patient with unilateral C5-T1 root avulsion. This indicates that this potential arises in stimulated peripheral nerve fibers. The second potential, although not consistently recorded in normal subjects, had an abnormally prolonged interpeak latency in 2 patients with cervical cord and medullary lesions. Therefore, it seems that it arises in the central nervous system, either in spinal cord or lower brain stem. The third potential was absent in 2 patients with medullary lesions and its interpeak latency was prolonged in 2 patients with brain stem lesions. It was recorded in 3 patients with thalamic lesions in whom subsequent potentials were absent. This suggests that this potential arises primarily in brain stem pathways. The negative potential was absent in 2 patients with cerebral lesions which did not appear to involve the thalamus which suggests that it arises in the thalamocortical radiations or cerebral cortex. Short latency evoked potential abnormalities correlated more with impairment of proprioception than with disturbances in appreciation of pain and temperature.

Short latency SEPs to median nerve stimulation: Comparison of recording methods and origin of components

Abstract Short latency SEPs recorded in scalp and cervical spine non-cephalic reference leads, cervical spine scalp and scalp-ear leads were obtained in 9 normal subjects and 20 patients in order to provide information concerning the generator sources of potentials recorded using the different derivations. Cervical spine non-cephalic reference leads yielded initially positive bi- or triphasic potentials, which reflect the ascending volley as it approaches the cervical recording electrode from the periphery (positive) and passes under the recording electrode in the spinal cord (negative). Scalp-non-cephalic reference recordings yielded up to 4 positive potentials (P 9 , P 11 , P 13 , P 14 ) followed by a negative potential (N 20 ). Evidence from both normal subjects and patients suggests the following origins for these components. P 9 primarily in proximal segments of stimulated median nerve fibers as they course from axilla to spinal cord, P 11 in spinal cord dorsal columns, P 13 in brain stem lemniscal pathways and P 14 in brain stem or diencephalic lemniscal pathways. Cervical spinal scalp leads yield up to 4 ‘negative’ potentials (N 9 , N 11 , N 13 , N 14 ). Evidence is presented which suggests the following origins for these components. ‘N 9 ’ is a positive potential which is more prominent over the scalp (P 9 ) and rostral cervical spine than it is over the caudal cervical spine. This component has the same origin as P 9 recorded from the scalp. N 11 is contributed to by the initial portion of the negative potential recorded by the cervical electrode which arises in the dorsal columns and a positive potential recorded by the scalp electrode (P 11 ). N 13 is also a composite potential contributed to by a portion of the negative potential recorded by the cervical electrode which reflects spinal cord synaptic activity and the P 13 potential recorded by the scalp electrode. The ‘N 14 ’ inflection is the P 14 potential recorded by the scalp electrode.

Somatosensory far field potentials: Studies in normal subjects and patients with multiple sclerosis ☆ ☆☆

Abstract Somatosensory evoked potentials to median nerve stimulation which arise in subcortical structures were recorded from the scalp of 15 normal subjects and 26 patients with definite multiple sclerosis (McAlpines criteria) in non-cephalic reference leads. In normal subjects, these subcortical events consisted of 3 positive potentials which were distributed widely over the scalp and were of similar amplitude at all scalp recording locations. In some subjects, these potentials were followed by another positive potential which was recorded predominantly over frontal central scalp regions. These potentials were followed by a larger negative potential which was most prominent over the somesthetic cortex contralateral to the side of stimulation. This negative potential is thought to reflect the arrival of the afferent volley in cerebral cortical elements. The criteria for abnormality in the patient group were (a) absence of components consistently recorded in normal subjects, (b) statistically significant component peak latency differences in patients compared to normal subjects, and (c) statistically significant differences in the amplitudes of the third positive and first negative potentials to stimulation of the left median nerve as compared with right median nerve stimulation. The response in all but one of the patients was judged to be abnormal. Absent components were observed in 17 patients, prolonged peak latency differences in 13 patients and component amplitude measurements were abnormal in 3 patients. Sequential recordings obtained in 5 of 9 patients revealed loss of components or latency changes. Evoked potential abnormalities were often found in the absence of either brain stem signs or clinically evident disturbances of specific sensory systems.

SHORT‐LATENCY SOMATOSENSORY EVOKED POTENTIALS TO MEDIAN AND PERONEAL NERVE STIMULATION: STUDIES IN NORMAL SUBJECTS AND PATIENTS WITH NEUROLOGIC DISEASE

SSEPs to median nerve stimulation which arise in the brachial plexus, subcortical and cortical structures can be recorded from the scalp. Abnormalities of these potentials have been found in patients with demyelinating disease and focal or diffuse disease of the nervous system. SSEPs to peroneal nerve stimulation which arise in rostral spinal cord, brainstem, and cerebral structures have also been recorded from the scalp. These methods can be expected to provide useful information in patients with certain neurological disorders.

Short‐latency somatosensory evoked potentials to median nerve stimulation in patients with diffuse neurologic disease

Short-latency somatosensory evoked potentials were found to be abnormal in 15 of 28 patients with diffuse neurologic disease of varying etiology and severity. These abnormalities often did not directly correlate with the presence or degree of clinical sensory impairment. They were similar to findings in patients with demyelinating and focal lesions of the nervous system. This suggests that the interpretation of these potentials can be done only in the context of the patients clinical assessment.

Hypernatremia and chorea A report of two cases

The appearance of transient, generalized chorea in conjunction with brief, symmetrical myoclonic movements is described in two adult patients with hypernatremia secondary to dehydration. The association of hypernatremia and chorea is rare, even in massive salt poisoning, and has not been described previously in adults. Since both patients recovered, no pathologic material was obtained; but a speculative commentary on the possible underlying pathophysiology is included.

Isolated complete post‐traumatic trigeminal neuropathy

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Reversible Cerebral Vasoconstriction Syndrome: A Rose by Any Other Name?

N EW NEUROLOGICAL ENTITIES, EITHER SYNdromes or diseases, continue to be described and defined in the 21st century. Neuromyelitis optica, postulated by some to be a variant of multiple sclerosis even in the late 20th century, has more recently been defined as a separate disease with its own pathogenesis, clinical description, diagnostic testing, and treatment. Reversible cerebral vasoconstriction syndrome (RCVS) has now been defined as a syndrome, but not a clear-cut disease entity. The syndrome typically presents with repeated thunderclap headaches over days to weeks. Cerebrovascular imaging reveals diffuse segmental constriction and dilatation of large and medium-sized intradural arteries. These abnormalities are transient and resolve within 3 months of clinical presentation. Convexity subarachnoid hemorrhage, intracerebral hemorrhage, seizures, and posterior reversible encephalopathy syndrome (PRES) occur in a minority of patients early, usually in the first week. Transient ischemic attacks and cerebral infarcts occur later. However, these complications are usually transient and resolve. Few patients are left with permanent sequelae. Results of cerebrospinal fluid testing are normal or show only a slight pleocytosis and elevated protein levels.