Symptomatic cataplexy.

Abstract

SUMMARYThe case is described of a man who developed attacks of cataplexy, narcolepsy, and sleep paralysis because of a microglioma which infiltrated the walls and floor of the IlIrd ventricle and the upper brain stem. The mechanisms by which the pathology is related to the symptoms are discussed.In 1880 Gdlineau coined the term 'narcolepsy' and related the clinical details of two patients who suffered from the condition, acknowledging that an account of the first had been published by Caffe in 1862. Henneberg (1916) described cataplexy with narcolepsy, and in the 1920s sleep paralysis became associated with the disease. Despite widespread interest and a large literature the cause remains unknown, and the vast majority of cases have no known structural basis. In the minority narcolepsy is said to be 'secondary' to various pathological conditions-to injury (Drake, 1949), to brain stem infarction (Van Bogaert, 1926), to third ventricular tumour (Fulton and Bailey, 1929), to polioencephalitis (Pohl, 1966)-or has occurred with other neurological disease, disseminated sclerosis (Ekbom, 1966;Berg and Hanley, 1963), and cerebellar haemangioblastoma (Tridon et al., 1969). We do not know of a case of primary narcolepsy coming to necropsy, and postmortem details of secondary narcolepsy are distinctly rare (Van Bogaert, 1926;Fulton and Bailey, 1929;Benedek and Juba, 1943; Pohl, 1966). Levin (1932)

The Pineal Gland, Cataplexy, and Multiple Sclerosis

“…Niemann-Pick's disease (Kandt et al, 1982). cerebral tumors (Ethelberg, 1949;Anderson & Salmon, 1977: Stahl et al. 1980Smith, 1983).…”

Electrophysiological brain stem investigations in idiopathic narcolepsy

“…Animal studies have demonstrated a prominent role of the brain stem and hypothalamus in the regulation of sleep and wakefulness and have led to the identification of neural generators and modulators of REM sleep in the dorsolateral pons and medial medulla oblongata [2,18,27,30,32,36]. In man, several case studies have reported symptomatic narcolepsy following acquired diencephalic lesions [3,29,34] and brain stem lesions of midbrain [4,10,23,37], pontine [23,24,31,33] and medullary [8] location. However, not all of these cases exhibited a classic narcoleptic syndrome, and some did not meet all diagnostic criteria of narcolepsy according to the International Classification of Sleep Disorders (ICSD).…”

Sleep and Wakefulness After Treatment for Craniopharyngioma in Childhood; Influence on the Quality and Maturation of Sleep

“…The craniopharyngioma develops from remnants of the embryonal hypophyseal-pharyngeal duct, located in the vicinity of the hypothalamus, the pituitary stalk and the optic chiasm. It has been known for long time that this area is important for the regulation of sleep and diurnal rhythms (17), and sleep disturbances secondary to tumors close to the hypo-thalamus and the 3rd ventricle have been repeatedly described (1,10,12,27,32). The suprachiasmatic nuclei (SNC), situated bilaterally just above the optic chiasm, act as endogenous regulators of the biological rhythm, receiving different signals directly from the optic tract (16,24).…”