Multiple averaged records to identify Aδ-fibers in sensory nerves.

Background: Existing methods identify only ≈10 Aδ-fibers in human sensory nerves per recording. This study examines methods to increase the detection of Aδ-fibers.

New Method: Two to 20 averages of 500 replicate responses to epidermal nerve stimulation are obtained.

Median amplitude and frequency analysis of sensory nerve responses to intraepidermal stimulation.

Background: In clinical practice, small myelinated sensory fibers conveying pain and other sensations, Aδ-fibers, cannot be examined with available nerve conduction study techniques.

New Method: Equipment available in clinical neurophysiology laboratories is used to record from human sensory nerves multiple averaged responses to non-painful stimulation of intraepidermal nerves. Ten averaged responses are analyzed in all possible pair combinations with an algorithm applied to a 0.

Slowly conducting potentials in human sensory nerves.

Background: In clinical practice, small myelinated sensory fibers, Aδ-fibers, conveying mainly pain and temperature sensations, cannot be examined with available nerve conduction study techniques. Currently, these fibers can only be examined with experimental or very specialized and not commonly available nerve conduction techniques, or only indirectly with cerebral evoked potentials.

New Method: This study uses equipment and methods available in clinical neurophysiology laboratories to record from human sensory nerves ≥1000 averaged responses to focal, non-painful stimuli applied by a special electrode to epidermal nerves.

[Nasojejunal enteral feeding tubes in critically ill patients. Successful placement without technical assistance].

Background: Critically ill patients with early enteral feeding seem to profit from post-pyloric administration. Two feeding tubes were studied that, due to their construction, are able to move into the duodenum without the necessity of technical support. The duration until successful positioning, time until total enteral feeding and possible complications were compared.

Clinical heterogeneity of familial spastic paraplegia linked to chromosome 2p21.

The clinical features of four families with autosomal dominant spastic paraparesis (FSP) are described, along with the results of linkage analysis to markers from the regions of chromosomes 2, 14, and 15 which are known to contain spastic paraplegia genes. All families had 'pure' spastic paraparesis (FSP), but the severity of symptoms varied widely among families, and other mild neurologic signs were observed in some subjects. Although no family individually yielded a lod score >3.

Ammonium ions abolish excitatory synaptic transmission between cerebellar neurons in primary dissociated tissue culture.

1. Transmitter glutamate is thought to be derived from glutamine via cleavage by glutaminase. NH+4 inhibits glutaminase.

Effects of NH4+ on reflexes in cat spinal cord.

1. In deeply barbiturate-anesthetized animals. NH4+ decreases spinal excitatory synaptic transmission by neuronal depolarization and subsequent block of conduction of action potentials into presynaptic terminals of low-threshold (presumably Ia-) afferents.

Ammonium decreases excitatory synaptic transmission in cat spinal cord in vivo.

1. Glutamine is thought to be a precursor of the pool of glutamate that is used as synaptic transmitter. NH4+ inhibits glutaminase, the enzyme presumed to cleave glutamine into glutamate in synaptic terminals.

The H-reflex in the encephalopathy due to ammonia intoxication.

Ammonia intoxication has been shown to decrease excitatory synaptic transmission in several regions of the central nervous system. To investigate the relation between an effect of ammonia on excitatory synaptic transmission and the behavioral depression in the encephalopathy due to ammonia intoxication, this study examined in the rat the effects of ammonia intoxication on the H-reflex, the behavioral and neurological signs of the encephalopathy due to ammonia intoxication, and correlated the effects on the H-reflex with the signs of encephalopathy. Ammonia intoxication abolished the H-reflex without affecting the M-response.

Synaptic transmission in ammonia intoxication.

Ammonia intoxication allegedly plays a significant role in the pathophysiology of hepatic encephalopathy. In order to understand the pathogenesis of this encephalopathy it is necessary to know the effects of ammonia on the mechanisms by which neurons communicate, i.e.

Porta-caval shunting changes neuronal sensitivity to ammonia.

The relations between an effect of ammonia on postsynaptic inhibition, the amount of ammonium acetate i.v. to obtain this effect, and the tissue concentrations of NH4+ and glutamine were investigated in the cerebral cortex of cats without and with portacaval shunts.

Ammonia intoxication: effects on cerebral cortex and spinal cord.

The effect of an acute systemic ammonia intoxication on the metabolic states of the cerebral cortex and the spinal cord of the same animal was studied in the cat. The intravenous infusion of ammonium acetate (2 and 4 mmol/kg body weight/30 min) increased the gross levels of tissue NH4+, glutamine, glutamine/glutamate ratio, lactate, and the lactate/pyruvate ratio in the cerebral cortex and the spinal cord. Pyruvate increased, but significantly only in the spinal cord; aspartate decreased, but significantly only in the cerebral cortex.

Pathophysiology of ammonia intoxication.

Ammonia intoxication affects postsynaptic inhibition and disturbs inhibitory neuronal interactions. This study investigated whether or not the effect of ammonia on postsynaptic inhibition was associated with a change of the EEG, i.e.

Ammonia, postsynaptic inhibition and CNS-energy state.

Ammonia intoxication decreases the hyperpolarizing action of postsynaptic inhibition. This study examines the metabolic state of the spinal cord during this effect of ammonia intoxication on spinal motoneurons. ATP, ADP, AMP, the adenylate energy charge, glucose, PCr, pyruvate, alpha-ketoglutarate and glutamate were unchanged during the effect of ammonia on the hyperpolarizing action of postsynaptic inhibition.

Ammonia intoxication and hyperpolarizing postsynaptic inhibition.

Systemic ammonia intoxication abolished the hyperpolarizing action of postsynaptic inhibition in the CNS at tissue concentrations of NH+4 which are sufficient to produce the earliest signs of encephalopathy. Therefore, the action of NH+4 on hyperpolarizing postsynaptic inhibition has to be considered as the cause, or as a contributing cause, of the encephalopathy due to systemic ammonia intoxication.

Ammonia and methionine sulfoximine intoxication.

Intoxication with ammonium acetate abolished the suppression of action potential generation by cortical postsynaptic inhibition, i.e. produced 'disinhibition', due to the inactivation of neuronal Cl- extrusion.

Ammonia and disinhibition in cat motor cortex by ammonium acetate, monofluoroacetate and insulin-induced hypoglycemia.

Ammonia intoxication abolished the suppression of action potential generation by cortical postsynaptic inhibition due to the inactivation of neuronal Cl- extrusion. The disinhibition by ammonia intoxication occurred when ammonia concentrations in the cerebral cortex were increased to 320% of normal. Fluoroacetate poisoning and insulin-induced hypoglycemia, which are known to increase ammonia concentrations in the CNS and previously have been shown to inactivate Cl- extrusion in spinal motoneurons, abolished the suppression of action potential generation by cortical postsynaptic inhibition like ammonia intoxication.

Anticonvulsant action of diazepam: increase of cortical postsynaptic inhibition.

The action of intravenously administered diazepam (Valium) on postsynaptic inhibition was studied in cat motor cortex. The efficacy of postsynaptic inhibition of pyramidal tract cells was measured as the ability to suppress action potential generation. Diazepam increased the suppression of action potentials by inhibition.

[Thyroid hormones and thyrotropin in liver and kidney insufficiency].

In 22 patients with hepatic or renal insufficiency the serum concentrations of trijodothyronin, thyroxine and thyrotropin and also the T4-binding capacity of TBG were determined. The mean serum T3 concentration was found to be significantly lower in patients with hepatic coma when compared with euthyroid subjects. In the cases of renal insufficiency the serum T3 concentrations were in the normal range.