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What I found...
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In reading all that everyone had to say, it seemed to me that I remembered reading quite some time ago that there were other possible causes of cataplexy other then narcolepsy.. so I did some research. This is what I found (second paragraph may be of most interest):
http://www.scholarpedia.org/article/Cataplexy (for full article)
Despite its primary association with narcolepsy, cataplexy is considered secondary when it is due to specific lesions in the brain that cause a depletion of the hypocretin neurotransmitter. Secondary cataplexy is associated with specific lesions located primarily in the lateral and posterior hypothalamus. Cataplexy due to brainstem lesions is uncommon particularly when seen in isolation. The lesions include tumors of the brain or brainstem and arterio-venous malformations. Some of the tumors include astrocytoma, glioblastoma, glioma, and subependynoma. These lesions can be visualized with brain imaging, however in their early stages they can be missed. In children cataplexy may alert the clinician to the presence of a tumor, particularly craniopharyngioma. This tumor accounts for 9 percent of all pediatric intracranial tumors [25]. In craniopharyngiomas, the onset of cataplectic symptoms is between 5-10 years of age, which is earlier than the peak of narcolepsy with cataplexy in children around the second decade between 12-18 years.
Other conditions in which cataplexy can be seen include ischemic events, multiple sclerosis, head injury, paraneoplastic syndromes, and infections such as encephalitis. Cataplexy may also occur transiently or permanently due to lesions of the hypothalamus that were caused by surgery, especially in difficult tumor resections. These lesions or generalized processes disrupt the hypocretin neurons and their pathways. The neurological process behind the lesion impairs pathways controlling the normal inhibition of muscle tone drop, consequently resulting in muscle atonia. Several reports have documented that damage to the lateral and posterior hypothalamus resulted in a loss of hypocretin producing neurons and the subsequent development of excessive daytime sleepiness and cataplexy [26, 27].
Cataplexy is tightly associated with the hypocretin neurotransmitter deficiency. Patients presenting with excessive daytime sleepiness, low to absent CSF hypocretin-1 level, and positive HLA DQB1*0602 halotype will most definitely have cataplexy. In children, it is important to rule out causes of secondary cataplexy. Cataplexy is treated with antidepressants such as tricyclics and serotonin reuptake inhibitors that enhance monoaminergic neurotransmission by inhibition of monoamine reuptake of NE and 5-HT. The newest compound in the treatment of cataplexy is sodium oxybate, but its mechanism of action is unclear. Cataplexy is commonly associated with narcolepsy. Primary cataplexy is a life long condition and can be disabling for the individual. Therefore, accurate diagnosis, education, and treatment are essential in order to allow the individual to have a normal and active lifestyle.
So, while it seems hypocretins is a common factor with N and C.. there are still other conditions that cataplexy can show up with. Don't know if this will help at all but thought it should be posted. Bless you and your daughter.