This review focuses on rodent models of tremor, particularly those induced by pharmacological agents. Harmaline is one of the most frequently used tremor-generating drugs and harmaline-induced tremor is regarded as a model of essential tremor. Harmaline acts on inferior olive neurons, causing enhanced neuronal synchrony and rhythmicity in the olivocerebellar system. In addition, it selectively induces cerebellar Purkinje cell death, speculatively because of excessive glutamate release from nerve terminals of the olivocerebellar system onto Purkinje cells. Systemic administration of cholinomimetics can also produce generalized tremor, and muscarinic receptors on striatal neurons are thought to be the best candidate for the tremor-generating mechanism. On the other hand, dopaminergic neurotoxins, which are used in models of parkinsonism, have yet to be used for experimental analysis of tremor, because tremors induced by dopamine depletion in rodents are less remarkable than those induced by harmaline or cholinomimetics. Recently developed gamma-aminobutyric acid (GABA)(A) receptor alpha-1 subunit knockout mice exhibit postural and kinetic tremors, and clearly reproduce the features of essential tremors. Although from a phenomenological point of view, rodent models of tremor cannot entirely mimic human tremor disorders, they have useful advantages in the analysis of pathophysiological mechanisms underlying tremor. Development of convenient and reproducible methods for evaluating rodent tremor is therefore recommended.

Objective There is growing interest in the use of transcranial sonography (TCS)

We report two patients with unilateral resting and postural tremor of the upper limb as a delayed manifestation of thalamic stroke. Neuroradiologic examination showed a lesion in the posterolateral thalamic region in both patients, but with no obvious involvement of the brainstem, the cerebellum, or the cerebellar outflow tract to the thalamic ventrolateral nucleus.

No abstract

Our objective was to evaluate diaphragm thicknesses during respiration by ultrasonography, and compare with conventional measurements of respiratory functions in patients with amyotrophic lateral sclerosis (ALS). Thirty-six consecutive ALS patients and 19 age-matched healthy volunteers participated. Ultrasonography of the diaphragm in the zone of apposition was performed. Maximal diaphragm thickness during the maximal inspiratory effort (DTmax) and minimum diaphragm thickness at the end expiratory position (DTmin) were measured using ultrasonography. The thickening ratio (TR), defined as the ratio of DTmin to DTmax, was calculated. All patients underwent conventional pulmonary function testing. Arterial blood gas analysis was also performed. The diaphragm was clearly identifiable by ultrasonography. DTmax, DTmin and the TR were all significantly decreased in ALS patients with %VC (vital capacity) < 80, compared with those in either ALS patients with %VC ≥ 80 or healthy controls. DTmax, DTmin and the TR were all significantly correlated with %VC. In addition, significant inverse correlations were found between all three parameters and pCO(2). The inter-observer reliability of measurements of diaphragm thickness was high. In conclusion, sonography of the diaphragm can provide additional or complementary information for assessing respiratory functions in patients with ALS.