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Tetanus toxin at doses of 2-2000 mouse MLD/kg was injected into the gastrocnemius muscle of the left hind limb of the cat. Acute experiments were performed at various times thereafter, when the intoxicated hind leg was strongly extended. Presynaptic inhibition of the monosynaptic reflex (MSR) of gastrocnemius motoneurones was tested by applying conditioning single electric stimuli to the antagonistic deep peroneal nerve. In most intoxicated animals the delayed inhibition of the MSR could still be observed at time intervals typical for presynaptic inhibition. However, the amplitude of the MSR often showed a strong toxin-induced facilitation at about 30 msec after the conditioning stimulus which could mask the presynaptic inhibition and sometimes made it difficult to observe it at all. After spinal transection at the Th1 level the inhibition could be better observed in such cases. Further evidence for the resistance of the presynaptic inhibitory system against the tetanus toxin in the given dose range was given by recordings of distinct dorsal root potentials which were abolished, together with the MSR inhibition by i.v. injection of picrotoxin. It is concluded that the mechanism of presynaptic inhibition remains intact or is even lengthened during local tetanus after i.m. injection of moderate, clinically relevant, toxin doses.

In a case of cephalic tetanus the amplitudes and the latencies of the compound action potentials recorded from the facial muscles after stimulation of the facial nerve at the mastoid were not significantly different on the two sides. With repetitive stimulation at 30/sec a pathological facilitation was observed on both sides. The blink reflex bilaterally had normal latencies but the amplitudes of the reflex potentials were always significantly lower on the paretic side. It is concluded that facial palsy in cephalic tetanus is mainly due to a functional block of conduction in the course of the peripheral nerve whereas the disturbance of neuromuscular transmission probably has little importance in these cases.

Bradycardia, sinus arrest, and second-degree atrioventricular block developed in 2 dogs with tetanus. Clinical signs attributable to bradycardia were not apparent. Administration of atropine resulted in resolution of the arrhythmias. Both dogs responded well to supportive treatment; the bradycardia resolved within 4 days of onset without specific treatment. Tetanus should be included in the differential diagnosis when increased neuromuscular excitability and bradycardia are evident, as is found in toxicity with acetylcholinesterase inhibitors, increased intracranial pressure, and other neurologic disorders.

The cardiovascular instability in some cases of severe tetanus is due to increased circulating catecholamines. In 15 patients with this complication of tetanus, labetalol, a drug with alpha- and beta-peripheral adrenergic blocking properties, was used in management. The drug was administered orally, by i.v. bolus or by continuous infusion. Wide variation in dosage was needed both from case to case and in the same patient during the course of his disease. In most cases the pulse and blood pressure were reduced by labetalol, although their variability was not much improved. The effect on the cardiac output and systemic vascular resistance ranged from modest reduction in both, to marked effect on cardiac output without any change in systemic vascular resistance. The alpha-adrenergic blockage of labetalol is known to be less powerful than the beta-blocking effect, and this property could be a disadvantage in the management of sympathetic overactivity in tetanus.

In twenty-eight patients suffering from tetanus, renal function was evaluated from admission for a period of 2 weeks. Investigations included daily blood urea, osmolality and creatinine and urinary osmolality and sodium. Free water clearance (CH2O) was calculated. The patients were divided into those requiring tracheostomy and sedation alone (Group I) and those with more severe tetanus requiring total muscle paralysis and IPPV (Group II). The latter group also had evidence of sympathetic nervous overactivity (SOA). Daily blood urea, serum creatinine and osmolality showed no significant difference between the two groups except during the phase of uremia. Mean urinary sodium was significantly different between the two groups (p less than 0.001). Four patients in Group II developed an abnormal plasma urea (Group IIb). In one patient the rise in urea followed resuscitation from cardiac arrest and the remaining three patients had in common severe cardiovascular instability associated with SOA. All four patients were non-oliguric during the phase of uremia. Only one patient with renal failure survived, compared with a 75% survival in the patients with SOA without renal failure and a 100% survival in Group I. Tetanus complicated by renal failure has a poor prognosis.

Brainstem reflexes have been studied electrophysiologically in six patients with generalized tetanus. The selective impairment of reflexes with long polysynaptic pathways supports the assumption of an interneuronal dysfunction in tetanus. The behaviour of proprioceptive reflexes suggests that hyperactivity of gamma-motoneurons contributes to the rigidity in an early stage of the disease.

From 1969-1985, 106 people contracted tetanus in Finland. The outcome of the disease was good in 78 cases (returned to work), poor in 27 (12 died, 5 institutionalized and 10 retired) and unknown in 1. Poor outcome was the result of a disease requiring respirator treatment. Other clinical factors significantly correlated with poor outcome were blood pressure lability, hyperglycemia, hyperthermia, tachycardia and anticoagulation therapy. Forty people who were representative of the whole series with regard to sex, age and severity of disease attended a follow-up study on average 7 years and 4 months later. Forty age- and sex-matched controls had the same examinations, and compared with them, the 40 patients still had significantly more muscle fatigue and cramps, nervousness, decreased mental capacity and difficulties in balance, speech and memory. They also had more clinical findings, such as peripheral paresis, muscular atrophy, decreased or absent tendon reflexes and decreased mental capacity than the controls.

A total of 150 patients were treated for tetanus in the tetanus ward of the J. J. Hospital, Bombay, between October 1983 and January 1986. The complications of tetanus and the mode of management in the presence of restricted resources are outlined. Intensive care, proper nutrition, early tracheostomy and ventilator support in severe tetanus were chiefly responsible for an overall reduction in mortality from 30 to 12%. The mortality in severe tetanus was reduced from 70 to 23%. Sudden death due to unexpected cardiac arrest was an important complication in severe tetanus. We observed that an abrupt marked rise in rectal temperature (greater than 107 degrees F, 41.7 degrees C), if undetected, could lead to sudden circulatory collapse and death. Well-marked hypoxaemia was observed in all patients with severe tetanus, and was related to ventilation perfusion inequalities and to an increase in the true venous admixture (increased Qs/Qt) in the lungs. Bronchopulmonary infections and the adult respiratory distress syndrome added significantly to morbidity and mortality. Autonomic cardiovascular disturbances included bradycardia alternating with tachycardia, and hypertension which was either labile, paroxysmal or sustained. Persistent hypotension was of ominous significance. Amongst numerous complications involving other systems, sepsis and septic shock were associated with a high mortality.

Besides the characteristic disturbances of the motor nervous system symptoms indicating an overactivity of the sympathetic nervous system can complicate the course of severe cases of tetanus. These symptoms include fluctuating tachycardia and hypertension, electrocardiographic changes, sweating, constipation with development of paralytic ileus and metabolic disorders. These symptoms are comparable to these developing in patients with phaeochromocytoma. Elevated catecholamine levels in plasma and urine have been found in several patients with tetanus who developed these symptoms. The prolonged over-activity of the sympathetic nervous system is thought to contribute to the still considerably high mortality rate. Myocardial lesions observed at necropsy are comparable to those found in patients dying of phaeochromocytoma. These lesions are suggested to be associated with sudden death from arrhythmias or cardiac failure in patients with tetanus. For the protection of the organism against the overactivity of the sympathetic nervous system a treatment using the combination of beta-adrenergic receptor blocking agents and adrenergic neuron blocking agents has been introduced. A reduction of the mortality rate was achievable by this treatment. Experimental evidence is accumulating that the tetanus toxin affects not only the motor, but also the sympathetic and sensory neurons.

Two patients with tetanus are reported to illustrate the involvement of the sympathetic and parasympathetic nervous system respectively. Aspects of the autonomic manifestations of tetanus are illustrated and discussed.

A patient with tetanus had a labile blood pressure caused by marked fluctuations in systemic vascular resistance. During hypotensive episodes, mixed venous oxygen saturation decreased below 60%. Hemodynamic instability was controlled after institution of a continuous lumbar epidural local anesthetic block.

Twenty-four Turkish children who had had neonatal tetanus were evaluated by means of physical and neurological examinations and psychometric tests at four to 15 years of age. Enuresis, mental retardation and growth retardation were frequent findings. The prevention of neonatal tetanus is important not only because of the high mortality rate but also because of its sequelae.

To assess the peripheral nervous system involvement caused by tetanus 40 patients recovered from tetanus and their sex and age matched referents were submitted to electroneuromyography (ENMG). Clinical symptoms and signs of peripheral neuropathy were found in 6 patients, 3 of whom had other obvious aetiology than tetanus. EMG was examined of the masseters and three muscles in the extremities. Motor conduction velocities (MCVs) were examined of the median, ulnar and peroneal nerves, distal sensory conduction velocity (dSCV) of the median, ulnar and radial nerves and the sensory conduction velocity (SCV) of the median nerve. Repetitive stimulation was done to study the neuromuscular transmission. The patients had significantly longer motor distal latencies (DLs) and slower dSCVs and more frequent ENMG findings compatible with mono- or polyneuropathy than their referents. There was no systematical difference in the MCVs. These findings suggest that tetanus may cause toxic axonal polyneuropathy, sequels of which appear to be slight or subclinical and can be seen at a group level.

To assess the brain involvement caused by tetanus, we examined the EEGs of 39 patients recovered from tetanus and those of 39 sex- and age-matched controls. The patients had significantly more frequent and more severe EEG abnormalities than their controls. The most marked difference was in the occurrence of diffuse EEG abnormalities (P less than 0.05). Twenty patients had normal EEGs. EEGs of 14 patients (5 of whom in this follow-up) during acute tetanus showed abnormalities in 10 patients, marked in degree in 3 of those. EEG abnormalities started to improve after the acute phase of tetanus. It is concluded that EEGs of patients with tetanus are often abnormal and that EEG is helpful in revealing brain involvement in patients after tetanus.

Tetanus relapses are caused by reactivated tetanus spores which have remained in the region of the wound, and made possible by unsatisfactory immunisation during a tetanus infection. From previously communicated individual case reports, the frequency of relapse, the length of the interval and the type of course are grouped together and compared with a case of our own. Electromyography plays a decisive role in the differential diagnosis of clinically similar syndromes and hysterical reactions. The characteristic electrophysiological findings are presented from the example of our own patient. Finally the therapeutic consequences are pointed out.

In a 69-year-old man with severe tetanus, sympatho-adrenal overactivity was successfully treated with a lumbar epidural block. Cardiovascular disturbances were reduced and fluctuations in plasma catecholamines were decreased. The duration of other manifestations of tetanus was, however, not influenced by the epidural block in this case.

The effects of stimulation of carotid body chemoreceptors on blood pressure, heart rate and ventilation were compared in normal rats and rats with local or generalised tetanus toxicity induced by injection of the toxin. Carotid chemoreceptor stimulation in an increase in blood pressure and a decrease in heart rate in both control and tetanus rats. However, while chemoreceptor stimulation resulted in increases in ventilation of 115% and 123% in normal rats and rats with local tetanus respectively, the increase in rats with generalised tetanus was only 29%. The experiments indicate that normal rats and rats with tetanus toxicity exhibit identical pressor and heart rate responses to stimulation of carotid chemoreceptors whereas the ventilatory response is attenuated in the tetanus rats.

We report a case of tetanus associated with the syndrome of sympathetic overactivity. BP changes were associated with changes in systemic vascular resistance index (SVRI). Cardiac index (CI) varied independently from changes in SVRI and was correlated with the stroke volume. Oxygen consumption during the hypotensive periods was normal. Among several pharmacologic agents, only curare was effective in decreasing the severity and number of the hypertensive episodes. Physical stimulation of the patient rapidly reversed the hypotension. The potential mechanisms involved in producing these cardiovascular abnormalities are discussed.

We studied the use of continuous iv magnesium (Mg) infusion to control the sympathetic crises in a patient with severe tetanus characterized by pronounced autonomic nervous system instability. Our results suggested that Mg is a useful adjunct to the CNS depressants traditionally used. This therapy controlled the sympathetic crises and also suppressed the release of catecholamines, although Mg infusions alone appeared to be inadequate therapy.