Carl H. Gunderson

Nerve agents: A review

Nerve agents produce neuromuscular blockade and convulsions in exposed humans. Military personnel in areas of potential exposure take prophylactic pyridostigmine. They are instructed to self-administer atropine and pralidoxime at the first sign of nerve agent toxicity. The key to treatment of nerve agent poisoning is the administration of atropine in doses larger than is customary in most other disorders, repeated as often as needed. Mechanical ventilation may be required. Convulsions are treated with diazepam, but only after atropine has been administered.

The neurology clerkship core curriculum

Abstract—Neurologic symptoms are common in all practice settings, and neurologic diseases comprise a large and increasing proportion of health care expenditures and global disease burden. Consequently, the training of all physicians should prepare them to recognize patients who may have neurologic disease, and to take the initial steps in evaluating and managing those patients. We present a core curriculum outlining the clinical neurology skills and knowledge necessary to achieve that degree of preparation. The curriculum emphasizes general principles and a systematic approach to patients with neurologic symptoms and signs. The ability to perform and interpret the neurologic examination is fundamental to that approach, so the curriculum delineates the essential components of the examination in three different clinical settings. The focus of the curriculum is on symptom-based rather than disease-based learning. The only specific diseases selected for inclusion are conditions that are common or require urgent management. This curriculum has been approved by the national organization of neurology clerkship directors and endorsed by the major national professional organizations of neurologists. It is intended as a template for planning a neurology clerkship and as a benchmark for evaluating existing clerkships. It should be especially helpful to clerkship directors, neurology chairs, deans of medical education, and members of external accreditation groups.

Sleep deprivation seizures

Neurologists have long suspected that loss of sleep or irregularity of the sleep-waking cycle might contribute t o the production or precipitation of seizures in some individuals.’ >* However, there is little experimental evidence to support this and very few instances of seizures after sleep deprivation have been described.*>’ Seizures are common, and so is loss of sleep; their relationship in man has never been established. An opportunity t o test the relationship between sleep deprivation and convulsions was offered by a steady flow of soldiers who had seizures while they were processing through the personnel center a t Oakland Army Base (OAB), California. Most were young men who had just completed a 1 3 month tour in the Far East. During the excitement and dislocation of returning home, their sleep cycle had been disturbed for one t o five days. While they were processing a t OAB, each had a single grand ma1 seizure, usually witnessed by personnel familiar with such occurrences. History, neurologic examination, and laboratory studies revealed n o other characteristic abnormality. Thirty-eight such noneplept ic , nonalcoholic patients were admitted to Letterman General Hospital (LGH) from the OAB population between 1966 and 1968. Two similar patients were admitted from other sources. Comparison between certain subgroups of this patient population and the population a t OAB allowed us to 618 Neurology / Volume 23 / Ju ly 1973 show a statistically significant relationship between sleep deprivation and seizures. From these data it was also possible t o estimate the number of individuals susceptible to seizures after sleep deprivation in a population of apparently healthy young men.

Somatosensory evoked potentials and magnetic resonance imaging in syringomyelia.

Somatosensory evoked potentials (SEPs) to median and posterior tibial stimulation were obtained in 22 patients with syringomyelia. All patients had magnetic resonance imaging (MR) which defined the maximum transverse diameter of the syrinx as well as its longitudinal extension. SEP was abnormal in 16 (72%) patients. Median and posterior tibial SEPs were abnormal in 11 and 15 patients respectively. Both tests were abnormal in 10 patients. Ten patients showed absence of one or more central potentials (P/N13, N20, N22) and 7 patients demonstrated increased conduction times (N9-N20, P/N13-N20, N22-P40). The mean maximum transverse diameter of the syrinx was 7.5 mm in patients with normal SEPs and 16.2 mm in patients with abnormal SEPs. Abnormal SEP was observed in all 5 patients with loss of position sense, in 9 of 13 (69%) with loss of superficial pain and temperature, and 1 of 2 patients with motor deficit only. Central SEP abnormalities were observed in 3 of 5 patients with sensory deficits indistinguishable from a peripheral neuropathy and in 2 patients in the asymptomatic extremity. Three of 4 patients with syringomyelia and Chiari malformation had a normal SEP.

Carbamazepine‐induced orofacial dyskinesia

Extrapyramidal syndromes have been described after administration of phenytoin and primidone.1-4 Although asterixis, dystonia, and tremor have been described with carbamazepine (Tegretol)1,5-7 there is no report of orofacial dyskinesia. We report a case in which a dose-related lingual-facial-buccal extrapyramidal reaction occurred in association with carbamazepine intoxication.

EEG and neuroimaging localization in partial epilepsy

We have studied cortical localization provided by surface and sphenoidal electroencephalograms (EEGs) and that of computed tomography (CT), magnetic resonance imaging (MR) and single photon emission tomography (SPECT) in 58 patients with partial epilepsy. Each patient had EEG, MR and SPECT during a hospitalization period of 1-2 weeks. CT scans were obtained either during the same period or had been performed in the preceding year. EEG evaluation consisted of 3-5 days of continuous monitoring including video-telemetry and ambulatory recording as well as conventional EEGs with special electrode placements. Additionally 33 of 58 patients (55%) who were potential surgical candidates had sphenoidal recordings. All patients had an abnormal EEG which showed evidence of epileptic hyperexcitability. EEG abnormality was localized in 43 patients (74%). Neuroimaging studies were focally abnormal in 38 patients (66%); 12 CT (21%), 29 MR (50%) and 24 SPECT (41%). Thirty four of 43 patients with localized EEG had at least 1 focally abnormal neuroimaging study (79%), whereas 4 of 15 (27%) patients with non-localized EEG did so. Twenty-eight of 29 patients with focal MR (97%), 11 of 12 patients with focal CT (92%) and 20 of 24 patients with focal SPECT (83%) had a concordant focal EEG. EEG and neuroimaging localization agreed in all 15 patients in whom both MR and SPECT disclosed a concordant focal abnormality. This study demonstrates a significant (P less than 0.005) correlation between surface/sphenoid EEG and neuroimaging localization in partial epilepsy.

Somatosensory evoked potentials and magnetic resonance imaging in intraspinal neoplasms

Median and posterior tibial somatosensory evoked potentials (SEPs) were studied on 25 patients with pathologically proven intraspinal neoplasms, and the results were compared and correlated with the details of clinical examination and the information derived from magnetic resonance imaging (MR). MR was abnormal in all cases and in 23 of 25 (92%) demonstrated an intraspinal expansile lesion. SEP was abnormal in 19 of 25 patients (76%). Abnormal SEPs were found in 18 of 19 patients (94%) with cervical or thoracic neoplasms but only in 1 of 6 patients (16%) with the tumor in the thoracolumbar or lumbar region. SEP-MR correlation was significant (P less than 0.05) for thoracic intraspinal neoplasms where all 9 had an abnormal SEP showing a similar pattern of normal median and abnormal posterior tibial study. Clinically, all 7 patients with posterior column sensory deficits had abnormal SEP (100%). Abnormal SEPs were seen in 7 of 11 (63%) patients with spinothalamic deficits and in 4 of 8 (50%) of those with normal sensory examinations. Four of 9 patients (44%) with a normal neurological examination or an examination disclosing ambiguous results indistinguishable from a peripheral pathology had an abnormal SEP strongly suggesting a central sensory disorder. Comparison of preoperative and postoperative SEPs did not disclose useful prognostic information pertaining to the functional recovery.

Improvement of ataxic helmiparesis with trihexyphenidyl

In a patient with the syndrome of crural paresis and homolateral ataxia, administration of trihexyphenidyl resulted in improvement of disabling unilateral ataxia and gross intention tremor. Symptoms returned when drug therapy was interrupted. CT showed a radiolucent lesion deep in the parietal white matter close to the internal capsule.

The site of the lesion in acute deafness of multiple sclerosis--contribution of the brain stem auditory evoked potential test.

Two patients with multiple sclerosis experienced acute unilateral deafness during an exacerbation. The brain stem auditory evoked potential test (BAEP) of both patients revealed absence of all waves after wave I, on the side of the hearing loss. These findings strongly suggest that acute hearing loss in multiple sclerosis results from involvement of the eighth nerve close to the ponto-medullary junction.

5-Year Study of Incidence Rates of Hospitalized Cases of Head Injuries in the US Army

Incidence rates of hospitalized head injury cases in the US Army were calculated by age, race, and sex. Skull fractures and intracranial diagnoses were found almost exclusively in males. For concussion, white males were at about 1.5 times greater risk compared to black males, and white females were at about 2 to greater than 3 times the risk compared to black females. For other intracranial injury, males were at 1.25 to about 2 times increased risk compared to females, white males were at about 1.5 times risk compared to black males, and white females were at 1.5-2 times greater risk compared to black females. Ten percent of head injury cases had an alcohol-related additional diagnosis and 97% of these were found in males.