University of California, Davis, conference: Mild hypertension

Prevalence of "higher than normal" blood pressures in a community is inversely related to the magnitude of the elevation; the milder grades of elevation are far more prevalent. A multifactorially inherited tendency to develop hypertension is modulated by multiple environmental influences. Autonomic nervous and behavioral factors plausibly appear to contribute to the initiating mechanisms of hypertension; the associated hemodynamic changes and the resulting cardiovascular structural changes interact to perpetuate the process. The complex interaction of hypertension and atherosclerosis is further complicated by direct as well as secondary effects of antihypertensive drugs on atherogenesis. Attributable cardiovascular risk is generally proportional to the degree of hypertension across the entire range of elevated blood pressure; this kind of relationship holds also for normal versus subnormal blood pressure values. Pharmacologic lowering of blood pressure, however, does not confer proportional benefit. Thus, such lowering of blood pressure to normotensive levels does not reduce the risk level to that in the normotensive population. Therapeutic outcome is influenced by the interaction of blood pressure lowering, type of antihypertensive agents used, existing risk factors, and target organ damage. Benefits of lowering blood pressure in established mild hypertension (diastolic blood pressure greater than 95 mm Hg) are confirmed. Drug treatment of patients with lower diastolic blood pressure or with isolated elevations of systolic blood pressures continues to be controversial as does the choice of initial therapeutic agent(s). The large-scale experience of clinical trials encompassing the long-term risks and benefits of the drug treatment of mild hypertension is limited to the use of diuretics and adrenergic beta blockers. A variety of new and promising therapeutic agents for use as alternate choices for initial therapy needs to undergo comparative evaluation.     

Subakute Enzephalopathie mit epileptischen Anfällen bei einem Patienten mit chronischem Alkoholismus (SESA-Syndrom)

Zusammenfassung Subakute Enzephalopathie mit epileptischen Anf?llen bei Patienten mit chronischem Al-koholismus (SESA-Syndrom) ist neben h?ufigeren Erkrankungen wie Delirium tremens, Alkoholentzugskrampf, Wernicke-Korsakow-Syndrom, zentraler pontiner Myelinolyse und Marchiafava-Bignami-Syndrom eine seltene Alkoholfolgekrankheit. Multiple neurologische Defizite (Hemiparese, Hemianopsie oder Aphasie), rezidivierende fokale und generalisierte epileptische Anf?lle und periodische seitenbetonte steile Potentiale im EEG sind bei diesem Syndrom beschrieben worden. Ein 72j?hriger Patient mit chroni-schem Alkoholabusus wurde nach mehreren sekund?r generalisierten fokalen Anf?llen der rechten K?rperseite unter der Verdachtsdiagnose einer Enzephalitis aufgenommen. Die neurologische Untersuchung ergab eine globale Aphasie. Bei den Laboruntersuchungen zeigten sich erh?hte Werte für Gamma-GT und MCV. Sonstige Laboruntersuchungen und Liquoranalysen ergaben Normalbefunde. Im CCT und im zerebralen MRT zeigte sich eine Mikroangiopathie und eine Hirnatrophie. Trotz einer intraven?sen Behandlung mit Acyclovir und Vitamin B1 und einer 3fachen antikonvulsiven Therapie wurden weiterhin epileptische Anf?lle und eine Verschlechterung des Allgemeinzustandes beobachtet. Mehrere EEG-Untersuchungen ergaben periodische steile links parietookzipital betonte Wellen. Drei Monate nach Beginn der Symptomatik verstarb der Patient an einer Lungenentzündung. Das beschriebene klinische Bild entspricht den Kriterien des SESA-Syndroms.      

Botulinum toxin treatment of synkinesia and hyperlacrimation after facial palsy

OBJECTIVES—Toinvestigate the effects of injection of botulinum toxin type A (BTX A)into the orbicularis oculi muscle and lacrimal gland in patients withaberrant regeneration after facial palsy (facial synkinesias and hyperlacrimation).
METHODS—The effect ofthe toxin injection (on average 75 mouse units of BTX A) into theorbicularis oculi muscle on facial synkinesias was assessed on a fivepoint (0 to 4) scale in 10 patients with aberrant regeneration offacial nerve fibres after a peripheral facial nerve palsy. Six patientsunderwent a videographic control, which was assessed by a blindedindependent investigator. In two patients with hyperlacrimation anextra dose of botulinum toxin (on average 20 mouse units BTX A) wasinjected into the lacrimal gland and the effect was assessed using theSchirmer test and on a three point scale.
RESULTS—Botulinumtoxin type A had a good to excellent (grades 3 and 4) effect over anaverage of six months after 91% of injections. In 9% the injectionshad a moderate (grade 2) effect. Patients with hyperlacrimation showeda nearly complete recovery. There were no systemic side effects butfocal side effects due to a temporary weakness of the orbicularis oculimuscle were not uncommon.
CONCLUSIONS—Botulinumtoxin type A is the treatment of choice in motor and autonomic effectsof aberrant regeneration of facial nerve after a peripheral palsy. Therequired dose is similar to or slightly lower than the dose usuallyrecommended for hemifacial spasm.

     

Fulminante Mycoplasma-pneumoniae-assoziierte Meningoenzephalitis des Erwachsenen

Mycoplasma pneumoniae (M. pn.) commonly causes respiratory tract infections in humans. In a certain percentage of cases it may also be associated with various peripheral and central nervous system manifestations. We report a case of a 38-year-old previously healthy man who presented with hemiplegia and somnolence after he had suffered from a febrile respiratory infection 10 days earlier. Clinical features and laboratory investigations supported the diagnosis of an acute M. pneumoniae-associated meningoencephalitis. He was treated by an aggressive antibiotic and immunomodulatory regimen over the course of several weeks in the neurocritical care unit. Decompressive hemicraniectomy was performed due to life-threatening raised intracranial pressure. However, the patient recovered almost completely and presented with a mild neurological deficit after 3 months. Based on this case we give a review of the literature and discuss potential pathomechanisms and diagnostic approaches.     

Trends in the pathophysiology and pharmacotherapy of spasticity

Summary Spasticity develops after supraspinal or spinal lesions of descending motor systems, with obligate involvement of the corticospinal tract. Spasticity is characterized by an increase in muscle tone, which, in contrast to many other types of enhanced muscle tone, shows a marked velocity-dependent increase when the muscle is passively stretched. The pathophysiological mechanisms underlying this spastic muscle tone remain obscure. Three major causes are currently considered possible: (1) changes in the excitability of spinal interneurones; (2) receptor hypersensitivity; (3) formation of new synapses by sprouting. The latter mechanism could account for the long time course over which spastic muscle tone develops in hemiplegic or paraplegic patients, but there is no experimental evidence for this hypothesis. The electromyographic (EMG) gait analysis of patients with spasticity has thrown doubt on the common belief that the velocity-dependent increase in spastic muscle tone is evoked by stretch reflex activity and has led to the idea that spastic muscle tone resides in the muscle fibres themselves. While such a mechanism may contribute to the slowness of active movements in spastic patients, recent experiments on patients with spastic arm paresis have confirmed the classical view that the spastic muscle tone is related to the EMG activity evoked in the passively stretched muscle. This pathological EMG activity is seen during the entire range of the dynamic phase of the stretch, during which a normal muscle exhibits only an early, phasic burst at the highest stretch velocities employed. For the pharmacological treatment of spasticity, substances with different central or peripheral actions are available. Their assumed receptor actions are described, together with their main indications and side-effects. A new way to treat severe spasticity is the continuous intrathecal application of baclofen via an implantable pump. This application has the benefit that the sedative effect of baclofen when applied in high oral dosage is avoided.     

Contralateral early blink reflex in patients with facial nerve palsy: indication for synaptic reorganization in the facial nucleus during regeneration.

Fifty patients with Bell's palsy and 30 patients with etiologically different symptomatic peripheral facial nerve palsy were studied by means of electrically evoked blink reflexes 1-23 days after onset of paresis. Their results were compared with a normal control group of 30 healthy subjects. In a significant number of patients (64% in Bell's palsy and 53% in symptomatic facial nerve palsy) a contralateral early blink reflex response (R1) could be elicited upon stimulation of the normal side as compared to 13% in the control group. It is suggested that this result may be explained by synaptic reorganization of the facial nucleus leading to functional unmasking of pre-existing crossed trigemino-facial reflex pathways during regeneration. This view is in line with previous experimental data in animals on the time course of structural changes in the facial nucleus after lesioning of the ipsilateral facial nerve.     

Inhibition of extensorγ motoneurons by antagonistic primary and secondary spindle afferents

Summary About 2/3 of the efferents isolated from the medial gastrocnemius nerve were inhibited by longitudinal high-frequency vibration applied to the tendons of the non-contracting pretibial flexors (decerebrate cats). The inhibition appeared at 15–25 m amplitude of vibration and increased up to a maximum at nearly 100 m. Increasing the frequency of vibration from 100 to 300 Hz increased the inhibition. The reflex effects elicited by muscle vibration corresponded well in incidence and magnitude with those evoked by tetanization of the deep peroneal nerve at group I stimulus strength. The reflex disappeared when the nerve supply of the vibrated muscles was cut. The sensitivity of some pretibial proprioceptors to vibration was also tested. It is concluded that primary spindle endings of the pretibial flexors inhibit the extensor motoneurons. Some findings hint at a spinal pathway involving I a inhibitory interneurons.In addition, an inhibitory action of pretibial group II afferents, probably secondary spindle endings, on extensor efferents was demonstrated.The described fusimotor inhibition by antagonistic muscle spindle afferents is a further example of --linkage.