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The trigeminal neuralgia is characterised by paroxysmal appearing fulgurous stabbing pain. Its medical condition is caused through a local-circumscribed demyelinisation of the trigeminal nerve with consecutive conduction of salting impulses on afferent pain fibres. It is essential to differentiate the symptomatic from the idiopathic trigeminal neuralgia. As primary management, a pharmacological treatment with anticonvulsants is recommended in order to attenuate the ectopic-generated pain impulses. Different neurosurgical procedures are available in cases of resistance to therapy. Thereby, causal surgery in form of microvascular decompression is not only the operative treatment of choice, but because of the excellent results also a fundamental support of the theory of vascular compression. A comprehensive knowledge about diagnosis and management of trigeminal neuralgia is essential to treat patients efficiently and successfully. This synopsis summarises the current recommendations concerning diagnostics and therapeutic options.

Intralysosomal storage of polar lipids can be induced in rats by treatment with Chloroquine, which belongs to cationic amphiphilic compounds. The drug accumulates in lysosomes of cells of the peripheral nervous system and interferes with the catabolism of polar lipids. As a consequence the lysosomes are transformed into bodies which are characterized by an internal lamellated pattern. The lipids stored in the neuron cells are phospholipids. The purpose of the present study was to check up the chronological development of the structural and lipid histochemical alterations within neuron cells. A significant enlargement of perikarya was observed after treatment of 94 d. A moderate increase of lysosomes and phospholipids was noticed after 82 d. Some typical foam-cells were seen after a period of 250 d. Moreover, a special mitochondrial alteration was observed, which could express close correlations between phospholipid metabolism and damaged parts of mitochondria.