Hyperekplexia (/ˌhaɪ.pər.ɛkˈplɛk.si.ə/; "exaggerated surprise") is a neurological disorder characterized by a pronounced startle response to tactile or acoustic stimuli and an ensuing period of hypertonia.

Classic hyperekplexia is caused by genetic mutations in a number of different genes, all of which play an important role in glycine neurotransmission.

[4] The three main signs of hyperekplexia are generalized stiffness, excessive startle response beginning at birth, and nocturnal myoclonus.

[6] Other signs and symptoms of hyperekplexia may include episodic neonatal apnea, excessive movement during sleep and the head-retraction reflex.

Inhibitory glycine receptors are ligand-gated chloride channels that facilitate fast responses in the brainstem and spinal-cord.

Homomeric glycine receptors composed exclusively of alpha-1 subunits exhibit normal ion channel electrophysiology, but are not sequestered at the synaptic junction.

In comparison to the GlyT1 transporter, found mostly in glial cells, GlyT2 helps maintain a high concentration of glycine within the axon terminal of glycinergic neurons.

[citation needed] Gephyrin, an integral membrane protein believed to coordinate glycine receptors, is coded by the gene GPHN.

[15] Because of gephyrin's multi-functional nature, in mutated form it is not presumed to be a common genetic source of hyperekplexia.

[18] During attacks of hypertonia and apnea, the limbs and head may be forcibly manipulated towards the trunk in order to resolve the symptoms.