Abstract

Background and purpose Horner’s syndrome may result from a variety of central or peripheral lesions of the sympatho-excitatory pathway. Associated symptoms like focal anhidrosis or gustatory sweating are helpful to localize the lesion and to direct further neuroimaging procedures. The starch-iodine test according to Minor can reveal the extent of anhidrosis and therefore help to localize lesions of the sympathetic nervous system. Pharmacological pupillary testing, sympathetic skin response and autonomic testing may result in further information about the place of the lesion. Case report: We present a 44-year old male patient with clinical manifestation of right sided Horner’s syndrome after ipsilateral cervical disc herniation surgery at C6/C7. Horner‘s syndrome was accompanied by reduced sweating when exposed to heat and exercise, but enhanced gustatory sweating after consumption of spicy food, both only at the right side of the face. The patient also complained about severe neuropathic pain on his skin at the right side of his face and neck, exacerbating at times of changing weather and after performing exercise with the right arm. Neurological examination did not show any other pathological findings, especially no tonic pupils, no hyporeflexia, and no signs of a brainstem or other cerebral infarction. Laboratory diagnostics and lumbar puncture showed normal parameters. Sympathetic skin response of both hands and cardiac autonomic testing were also normal. Pharmacological pupillary testing with local cocaine showed significantly less pupil dilatation at the right side and therefore confirmed Horner’s syndrome. A sweating test was conducted to further localize the lesion of the sympatho-excitatory pathway. The starch-iodine test according to Minor was first performed after heat exposure and then again after eating spicy food (chili). It showed heat hypohidrosis on the right sight of the face, but neither on the right arm nor thorax. After intake of chili, gustatory sweating was only detected on the right facial hemisphere. MRI imaging of the brain and the cervical spine showed no abnormalities. By treatment with pregabalin, oxycodone/naloxone, and amitriptyline, we were able to reduce the neuropathic pain. A stellate ganglion block remains an option in case of refractory pain. Conclusion: By performing a starch-iodine test, we were able to localize the lesion of the sympathetic pathway at the area of the superior cervical ganglion of the sympathetic trunc. A damage at the stellate ganglion would have caused quadrant anhidrosis, while a central lesion e.g. at the hypothalamus would have caused hemianhidrosis. A more distal lesion at the carotid plexus results in only partial facial hypohidrosis or no hypohidrosis at all. We suspect a damage of the second order preganglionic sympathetic neuron, because gustatory sweating is most frequently described in preganglionic lesions. Despite the normal MRI scan, an association with the cervical surgery is probable. This case underlines the usefulness of “old” examination procedures like the starch-iodine sweat test in the topodiagnosis of focal dysautonomias like Horner‘s syndrome.

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