Acute syphilitic meningitis. Its occurrence after clinical and serologic cure of secondary syphilis with penicillin G.

Acute syphilitic meningitis developed in a 36-year-old man three months after apparently successful treatment of secondary syphilis with doses of penicillin G benzathine recommended by the current Centers for Disease Control guidelines. He was then treated with high-dose intravenous penicillin G sodium, with resolution of symptoms and cerebrospinal fluid abnormalities. Although other instances of neurosyphilis following adequate therapy for early syphilis have been reported, in most cases reinfection cannot be convincingly excluded. We believe this patient represents a particularly well-documented example of progression to neurosyphilis, despite recommended therapy with penicillin. A review of recently reported cases suggests that progression of syphilis, despite "appropriate" therapy, is not an isolated event.

Effect of pulmonary vascular pressure on lung lymph flow following seizures.

The effect of elevated baseline pulmonary vascular pressures on systemic and pulmonary vascular sequelae of prolonged seizures was studied in sheep. Five animals with seizures induced after baseline left atrial pressure elevations of 25 mm Hg were compared with animals treated with seizures alone. Seizure-induced elevations from baseline of systemic and pulmonary vascular pressures were identical in the two groups both in height and duration. In animals with left atrial balloon inflation prior to seizures, however, the peak pulmonary arterial and left atrial pressures were the sum of baseline elevation (induced by left atrial balloon inflation) and the seizure-induced pressure elevation. Accordingly, the resultant pulmonary vascular pressure and resultant pulmonary lymph flow elevations, were substantially greater in these animals with elevation in baseline pulmonary vascular pressures. Therefore, patients with pulmonary vascular hypertension are at greater risk for pulmonary edema during seizures.

Systemic and pulmonary vascular pressures during generalized seizures in sheep.

The systemic vascular response to seizures is known but information on the hemodynamics of the pulmonary circulation is lacking, clouding an understanding of the pathophysiology of postical pulmonary edema. We investigated this problem using electrically induced single seizures and bicuculline-induced status epilecticus in halothane-anesthetized sheep. Aortic, pulmonary arterial, and left atrial pressures were recorded throughout the seizure activity, and the responses of the systemic and pulmonary pressures were compared. All monitored pressures rose precipitously with the onset of seizures. In all types of seizure the pulmonary pressure elevation was brief, lasting only one-third as long as did the systemic. Pulmonary microvascular pressures rose well above the level of plasma oncotic pressure. Pulmonary vascular pressures were elevated in proportion to the duration of the seizure stimulus, while the systemic response did not so vary. Cervical spinal cord transection abolished all systemic and pulmonary vascular response to seizures, demonstrating ultimate neural mediation.

Pulmonary lymphatic flow alterations during intracranial hypertension in sheep.

The role of intracranial hypertension in the genesis of neurogenic pulmonary edema was studied in 25 sheep; cardiopulmonary hemodynamics (aortic, pulmonary arterial, and left atrial pressures and cardiac output) and fluid and protein movement across the pulmonary capillary bed (efferent pulmonary lymph flow and lymph/plasma protein ratio) were monitored. Only when intracranial pressure was raised to equal the baseline mean systemic pressure (75 to 120 Torr) did we observe the expected Cushing response of increased aortic pressure, or any alteration in pulmonary hemodynamics or fluid movement. When pulmonary changes did occur, they included an increase in pulmonary arterial pressure of between 5 and 15 Torr without any notable rise in left atrial pressure, and a sustained doubling of the pulmonary lymph flow with no dilution of the lymph/plasma protein ratio. In 3 additional animals cerebral ischemia alone produced an elevation in systemic pressure (74 Torr over baseline) without change in pulmonary arterial pressure, left atrial pressure, or pulmonary lymph flow. Thus, intracranial hypertension and ischemia both affect systemic pressure, but only the elevated intracranial pressure is followed by changes in the pulmonary circuit. We suggest that these changes in pulmonary vascular pressure, independent of changes in left atrial pressure, produce increased pulmonary transcapillary fluid flux that may result in neurogenic pulmonary edema.

Left atrial pressure elevation recreates the altered lung lymph flow of seizures.

We compared the effects of elevated left atrial pressure of central nervous system origin (bicuculline-induced seizures) with an identical pulmonary vascular pressure elevation induced in six sheep by inflation of a balloon in the left atrium. The degree and duration of the consequent elevation in pulmonary lymph flow and the alteration in protein movement in the two groups was identical. Alterations in pulmonary fluid and protein flux resulting from generalized seizures can be explained by the pressor response alone; specific brain-lung neural interactions need not be postulated.

Elevated pulmonary lymph flow and protein content during status epilepticus in sheep.

The pathophysiology of postictal pulmonary edema was investigated by inducing seizures with bicuculline in nine paralyzed, halothane-anesthetized sheep and measuring of pulmonary lymphatic flow, pulmonary arterial and left atrial pressures, and lymph and plasma albumin concentration. Pulmonary microvascular pressure and transcapillary albumin conductance were calculated. Seizures transiently (less than 15 min) elevated microvascular pressure in all animals; lymph flow increased greater than twofold in response to the increased hydrostatic driving force. However, the elevation in lymph flow, with a stable lymph-to-plasma protein ratio and doubled transcapillary albumin conductance, persisted for the duration of the experiment, more than 3 h after microvascular pressure returned to base line. These changes were neurally mediated because they were blocked by cervical spinal cord transection in four additional animals.