George W. Paulson

Overdose of lioresal.

This is the first reported case of a major overdose of Lioresal (baclofen or CIBA BA-346467). A 29-year-old woman with known Huntingtons disease took from 900 to 970 mg of Lioresal, a cogener of gamma amino butyric acid (GABA) used experimentally to treat muscle spasm. She was admitted in deep coma with absent brain stem reflexes and without spontaneous respiration, and she required cardiovascular support. Her pupils were fixed at 3 mm and unreactive for 48 hours. She continued to require intensive support for a total of 72 hours and had one seizure during the recovery phase. Her eventual recovery was complete. No specific antidotes are currently available for overdose of Lioresal and supportive care is the only method of treatment for overdose.

The rigid form of Huntington's chorea

THE RIGID FORM of Huntington’s chorea has been recognized for years and is usually seen as a sporadic case within a more typical choreic kindred. The rigid form has been considered a “biotype”1 of the more usual hyperkinetic and hypotonic form, although this concept is disputed.2 Discovery of a family in which the disease initially appeared to consist exclusively of a dominantly inherited dystonic process with ocular and mental abnormalities beginning in childhood led to intensive study of two afflicted members. Later discovery of a distant relative with classic Huntington’s chorea clarified the diagnosis. Nevertheless, the distinct and consistent findings in the initial

THE AVIAN EEG: AN ARTIFACT ASSOCIATED WITH OCULAR MOVEMENT.

Abstract 1. 1. An artifact in the EEG of chickens and several other bird species is reported and various attempts to determine its origin are described. It usually consists of rhythmic bursts of high voltage waves at 12–25 c/sec which are best detected by electrodes near the eyes. 2. 2. The artifact correlates with unilateral or bilateral nictitating membrane movement and is probably related to eyeball oscillation.

Cerebral and spinal fluid anaerobism during circulatory arrest

RESTRICTION of canine cerebral circulation leads to an accumulation of tissue lactate proportional to time up to about ten minutes of total substrate deprivation.1 Following severe cerebral stress of almost any etiological category with or without obvious cerebral nutrient and oxygen deficiency, cerebrospinal fluid (CSF) lactate levels have been noted to be elevated., Following restoration of circulation after vascular interruption, CSF lactate levels are also increased.3 Both the rapidity of lactate egress from brain tissue to CSF and the absolute amount of lactate in CSF during acute ischemia are unknown. Since CSF lactate concentration may be a measure of “brain death,” knowledge of CSF lactate concentration with known cerebral tissue lactate (CTL) accumulation may be valuable during an extended and known period of circulatory deprivation. Also, such comparison may afford information regarding the mechanism and rapidity of the transfer of this important metabolite across the brain-CSF barrier. CSF has been considered representative of brain extracellular space for many constituent elements, and CSF lactate levels have been utilized to indicate cerebral metabolic pe r fo r rnan~e .~ ,~ This investigation casts doubt upon the validity of the CSF lactate content, during extended circulatory arrest, as being entirely representative of conditions existing within brain tissue. Also, relative rates of lactate accumulation in brain, CSF, and blood have been substantiated.

Cerebrospinal fluid lactic acid in death and in brain death.

This is a report of cerebrospinal fluid (CSF) lactic acid in patients with “brain death,” in cadavers, and in living patients with neurological disorders. Earlier studies documented normal CSF lactic acid levels and reported elevated values in patients with subarachnoid hemorrhage and meningitis, and values were sometimes higher in nonsurvivors.’ ,z Transient increases in CSF lactic acid can occur with hyperventilation, possibly due to brain vasoconstriction and i ~ c h e m i a . ~ ~ These and other studies indicate that lactic acid crosses the normal blood-CSF barrier slowly from either direction. It can be postulated that in the absence of meningeal inflammation, CSF lactic acid reflects brain metabolism better than internal jugular or sagittal sinus lactic acid levels. In view of these concepts, it seemed likely that abnormalities in CSF lactic acid would be noted if the brain was irreversibly damaged; therefore, this study was undertaken. Although changes in CSF lactic acid after death have not been reported, earlier studies from this hospital noted a marked increase in the potassium, beta-glucuronidase, and acid phosphatase after death as well as a particularly consistent decrease in CSF bicarbonate in cadavers.8 The reduction in bicarbonate appeared to be due to an increase in the partial pressure of carbon dioxide and secondary to an increase in the lactic acid concentration of CSF. This study summarizes our data regarding CSF lactic acid in living and dead patients.