The neurobiochemical basis of motor inhibition and muscle tonicity in some tension syndromes, especially in patients with a state of wood stiffness, is mainly elevated dopamine activity. The efficacy of sulpiride in improving catatonia has been relatively satisfactory in the past, especially with sedation therapy, but there are still clinical reports of severe extrapyramidal reactions or exacerbation of catatonia symptoms. Although sulpiride has a specific high affinity for receptors and some effect on dopaminergic neurotransmitters, it has no significant effect on r-aminobutyric acid. Therefore, in the actual clinical application of some patients with xylophobia, there are still many that do not improve quickly in a short period of time. The neurobiochemical alterations in patients with the catatonia syndrome are characterized by high concentrations and imbalance of various central neurotransmitters. Aminergic nerves account for 70% to 80% of the central nervous system. Among them, GABAA neurons are the main inhibitory neurotransmitters, which play an important role in the process of facilitation and inhibition of human movement. Diazepam interacts with the GABAA chloride fraction on the nerve cell membrane to increase the chloride ions entering the cell, causing the cell membrane to be supercharged and producing the ignition effect of the inhibitory neurotransmitter, which exerts a strong anti-excitatory effect by inhibiting the neuronal production, reducing muscle tone and maintaining a certain state of muscle relaxation. Given that benzodiazepines have good efficacy in surgical rigidity and have an earlier onset of action than sulpiride6, it may be worthwhile to try them in some patients with tension syndromes in which some antipsychotic drugs are not effective or are poorly tolerated.