Klazomania - Pathophysiology

Pathophysiology

Jankovic and Mejia's 2006 review indicated that autopsies of victims of the 1917 to 1926 encepahlitis lethargica pandemic revealed "neurofibrillary tangles and neuronal loss in the globus pallidus, hypothalamus, midbrain tegmentum, periaqueductal gray matter, striatum, and the substantia nigra".

Wohlfart et al hypothesized that klazomania originates in the periaqueductal gray matter in the mesencephalon. The vocalizing center in animals is located in the periaqueductal gray matter and a klazomania-like episode involving grunts and animal sounds can be evoked by electrical stimulation of this region. Wohlfart and colleagues hypothesized that the stimulation of the autonomic nervous system by the posterior hypothalamus is involved in klazomania, adding that klazomania resembles sham rage in animals, which is controlled by stimulation of the sympathetic nervous system. During klazomania, a person may experience pupil dilation, tachycardia, salivation, increased blood pressure, retraction of lips, barking, grunting, and rage just as an animal would if presenting sham rage. Bates and colleagues (1996) say that neuroimaging and pathology results do not support evidence of hypothalamic involvement similar to that found in sham rage.

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