Frank R. Freemon

Sleep patterns in a patient with a brain stem infarction involving the raphe nucleus

Abstract A patient with an infarction in the basis pontis had a decreased sleep time but a normal percentage of REM sleep. Autopsy revealed a well defined infarction destroying the pontine and midbrain portions of the raphe nucleus. This patients polygraphically recorded sleep patterns are similar to the sleep patterns of experimental animals with raphe lesions.

The effect of chronically administered delta-9-tetrahydrocannabinol upon the polygraphically monitored sleep of normal volunteers.

This study describes the effect of two weeks of delta-9-tetrahydrocannabinol (THC) administration upon normal sleep. The two subjects, two brothers in their 20s, slept in the laboratory for 27 consecutive nights and then, after four nights at home, for four additional nights. One subject, after an adaption night, received placebo for four baseline nights, 30 mg of THC for the next 14 nights, and placebo during four withdrawal nights. The other subject received placebo during this entire period. One year later the subjects alternated these conditions. The subjects had difficulty falling and staying asleep during the first two nights of placebo after 14 consecutive drug nights. This mild drug withdrawal insomnia was not accompanied by the increase of REM sleep which frequently accompanies withdrawal of other drugs. Starting after about a week of THC administration, and continuing for a week after drug discontinuance, there was a marked decrease in the type of sleep associated with slow waves in the electroencephalogram, nonREM sleep stages 3 and 4. The fact that prolonged, but not acute use, suppresses slow wave sleep indicates that this commonly used drug produces a poorly understood change in brain physiology.

Clinical Features That Predict Potentially Reversible Progressive Intellectual Deterioration

The records of 110 patients with progressive intellectual deterioration were reviewed, to identify any clinical features that might predict the presence of an underlying disease potentially reversible with specific medical, surgical, or psychiatric therapy. The 16 patients in whom the intellectual deterioration was caused by such underlying disorders showed a shorter duration of symptoms and less cortical atrophy on a computed tomographic scan than did patients with idiopathic dementia. The average for the patients with a treatable cause of progressive intellectual deterioration was not significantly different from the average age for patients with idiopathic dementia.

The effect of δ9-tetrahydrocannabinol on sleep

Five volunteers slept 8 to 15 consecutive nights in the laboratory with electroencephalogram, chin electromyogram, and eye movements monitored by the method originated by Dement and Kleitman. δ9-tetrahydrocannabinol (THC), 20 mg administered at bedtime decreased the amount of time spent in the REM or paradoxical phase of sleep. Abrupt withdrawal of THC after 4 to 6 consecutive nights of use produced a mild insomnia characterized by difficulty in falling and staying asleep but did not produce a marked REM rebound.

Interaction of physostigmine and delta-9-tetrahydrocannabinol in man.

To investigate the hypothesis that delta‐9‐tetrahydrocannabinol (THC), the major psychoactive ingredient of marihuana, acts by interfering with cholinergic brain mechanisms, 0.75 to 1.25 mg of physostigmine, a centrally active cholinergic drug, was given intravenously to 5 normal volunteers who had ingested 20 to 40 mg of THC 2 hours earlier. Physostigmine decreased the degree of tachycardia and conjunctival injection produced by THC. The major psychologic effects of physostigmine were amplification of the lethargy and somnolence which occur late in the course of THC intoxication. We interpret the lack of physostigmine counteraction of the peak psychologic effects of THC as evidence against the hypothesis that THC acts predominantly by an anticholinergic mechanism.

AN ELECTROENCEPHALOGRAPHIC STUDY OF THE EFFECTS OF MEPROBAMATE ON HUMAN SLEEP.

The effect of meprobamate on human sleep and dreaming was assessed in a double‐blind, placebo‐controlled study by means of all‐night electroencephalography. On nights when meprobamate was ingested in a dose of 400 mg. at 9:00 P.M. and 800 mg. at 12:00 A.M., normal subiects spent significantly less time in sleep accompanied by low‐voltage fast EEG waves and more time in sleep manifested by spindling in the EEG than when receiving placebo. The time spent in rapid eye movement periods, which are related to visual dreaming, was decreased by meprobamate. This study shows that meprobamate characteristically alters the amount of time spent in each sleep stage and significantly decreases inferred oisual dreaming. Comparisons are made between the changes in the human electroencephalogram during sleep produced by meprobamate and those produced by the barbiturates.

Delirium and Organic Psychosis

Delirium is a syndrome of abnormal mental function characterized by apprehension progressing to panic, confusion to disorientation, and misinterpretation of sounds to frank hallucinations. Usually present are abnormal movements such as tremor, twitches, and jerks. Epileptic seizures can occur. Table I summarizes the clinical symptomatology that defines the syndrome.

The first career of William Alexander Hammond.

Neurology in its modern sense was first studied in the well-known neurological institutions of France and England. In America, however, this new field of medicine was developed by a physician in a private practice, Dr. William Alexander Hammond. This article addresses the question how Hammond was able to limit his practice to neurology. It is argued that Hammond was a famous military physician before becoming the first practitioner of clinical neurology in America. This fame translated into a large referral base.

Chapter 38: American neurology.

The great formative event in the history of North America, the Civil War of 1861 to 1865, was the stimulus for the development of clinical neurology and the neurosciences. The first neurological research center on the continent was the US Army hospital at Turners Lane, Philadelphia, PA. Silas Weir Mitchell and his colleagues described causalgia (reflex sympathetic dystrophy), phantom limb sensation, and Horners syndrome (before Horner). The medical leader of the Northern army was William Hammond. After the conclusion of hostilities, he began a huge clinical practice in New York City. In the United States, clinical neurology began in private practice, unlike Europe, where neurology began in institutions. Hammonds textbook, which first used the term athetosis, was used by a generation of physicians who encountered patients with neurological signs and symptoms. Early in the 20th century, neurological institutions were formed around universities; probably the most famous was the Montreal Neurological Institute founded by Wilder Penfield. The US federal government sponsored extensive research into the function and dysfunction of the nervous system through the Neurological Institute of Neurological Diseases and Blindness, later called the National Institute of Neurological Diseases and Stroke. The government officially classified the final 10 years of the 20th century as the Decade of the Brain and provided an even greater level of research funding.

William Alexander Hammond: the centenary of his death.

In the United States, the field of clinical neurology began within the medical practice of a single physician, William Alexander Hammond. In the 1870s, this New York medical practitioner became the first American physician who limited his practice to patients who suffered from symptoms potentially due to dysfunction of the nervous system. From the experience of his huge practice, Hammond wrote the first American textbook of neurology. With Silas Weir Mitchell, he founded the American Neurological Association. The year 2000 marked the 100th anniversary of Hammonds death and stimulates this brief survey of his life.